Acute glomerulonephritis (agn)

1. BY-YOGESH A DENGALE 2nd M.Sc Nsg

2.  Acute glomerulonephritis is a common disease in children and it is one of the
diseases that are presented commonly with hematuria which means red urine
(blood in urine). Acute Glomerulo Nephritis in all probabilities results secondary
to a proceeding streptococcal (beta-hemolyticus type 12) infection of throat or
skin. A history of upper respiratory infection.
3.  Acute Nephritis or glomerulonephritis is an infective renal disease
characterized by sudden onset of hematuria, oliguria, edema and hypertension.
4.  Acute glomerulonephritis is an immune – mediated inflammatory disease of
the capillary loops in the renal glomeruli. The antigen – antibody complex
deposition within the glomeruli results in glomerular injury which is manifested as
hematuria, oliguria, edema and hypertension.
5.  The Kidneys are paired reddish and bean shaped organs located in the
peritoneum and the posterior wall of the abdomen. The kidneys are located
between the levels of the last thoracic and third lumbar vertebrae, a position where
they are partially protected by the eleventh and twelfth pairs of ribs. The right
kidney is slightly lower than the left because the liver occupies considerable space
on the right side superior to the kidney.
6. 1.Homostasis function-  Excreting wastes and foreign substances 
Maintenance of water balance  Maintenance of electrolyte balance 
Maintenance of acid base balance 2.Hemopoietic function 3.Endocrine function
4.Regulation of blood pressure 5.Regulation of blood calcium level
7.  More common in male than females.  Most common in preschool and early
school age children with a peak age of onset of 6-7 years.  Rare in children
under two years of age.  On average responsible for 2 to 4% of pediatric
admissions in India.  Accounts for about 90% of renal diseases in childhood 
Varies with the prevalence of nephritogenic strains of streptococci and the
likelihood of cross – infection.
8. 1.Presumed cause – antigen – antibody reaction secondary to an infection in the
body. 2.Initial infection:  Usually either an upper respiratory infection or a skin
infection, usually one to 3 weeks before the onset of symptoms  Most frequent
causative agent – nephritogenic strains of group - A beta – haemolytic
streptococcus (type 12), acute post – streptococcal glomerulonephritis (APSGN) is
the most common.
9.  Most cases are post infectious and have been associated with -Pneumococcal
-Viral infection -Acute post streptococcal glomerulonephritis is the most common
of the post infectious renal disease in childhood. -Streptococcal pharyngitis is more
common in the winter.
10. Urinary symptoms:  Decreased urine output  Bloody or brown – coloured
urine. Oedema:  Present in most patients Usually mild.  Often manifested by
Periorbital oedema in the morning  May appear only as rapid weight gain. 
May be generalized and influenced by posture.
11. Hypertension:  Present in over 50 per cent of patients.  Usually mild. 
Rise in blood pressure may be sudden.  Usually appears during the first four to
five days of the illness. Malaise Mild headache  Gastrointestinal disturbances,
especially anorexia and vomiting, often with abdominal and long pain.  Pallor 
Irritability  Lethargy  Dysuria  Fever
12.  History of illness and physical examination help in clinical diagnosis. 
The confirmation of diagnosis is done by the following: Urine examination: It
shows increased specific gravity, smoke dirty brown colour urine with reduced
total amount in 24 hrs. Mild to moderate or severe albuminuria is detected.
Microscopic examination reveals presence of red cells, WBCs, pus cells, epithelial
cells and granular cast. Proteinuria (3+ to 4+)
13. Blood examination:  Blood examination demonstrates increased level of
urea, creatine, ESR, ASO titer and anti – DNAase ‘B’. There is decreased level of
Hb%, serum complement and albumin in blood. Hyponatremia and hyperkalemia
may occur in persistent oliguria. Throat swab culture:  Throat swab culture may
show presence of beta – hemolyticus streptococcus in some children. Chest X-ray:
 It may show pulmonary congestion
14. AGN with impaired renal function as severe oliguria and azotemia needs
hospitalization for special attention. Mild oliguria patients with normal blood
pressure can be managed at home with OPD – based treatment. Treatment is
essentially symptomatic Monitoring:  The patient should be monitored closely
for the presence of hematuria, decreased urinary output, and signs of volume
overload like edema, hypertension and congestive heart failure.
15.  Daily record the general condition, edema, consciousness level, weight,
heart rate, respiratory rate, blood pressure, fluid intake and urinary output.  The
kidney function tests must be monitored at regular intervals. Bed rest:  It is
rarely indicated except during the acute phase when complications of acute renal
failure may be present.  Protect the child from fatigue and contact with other
respiratory infections.  Position:  In congestive heart failure or hypertension,
make the patient lie in a propped up position and provide oxygen.
16. Diet:  Diet should be arranged with restriction of protein, salt and fluid
intake, till oliguria and increased blood urea level persist.  Carbohydrate
containing food to be allowed freely.  The diet of the patient need not be
restricted routinely.  Fluid intake should be allowed in a calculated amount (i.e.,
total amount of previous day urine output in 24 hrs plus insensible losses to be
allowed to drink on that day).  Daily weight recording is important to assess the
increase and decrease of edema.
17. Fluid balance:  Regular measurement of vital signs, body weight and intake
and output is essential to monitor the disease’s progress and detect complications
that may appear at any time during the course of the disease.  A record of daily
weight is the most useful means to assess fluid balance and should be kept for
children treated at home and for those who are hospitalized.  Sodium and water
restriction is useful when the output is significantly reduced (< 2 to 3 dl/24hr.) 
In these children the water allowed is equivalent to the calculated insensible loss
plus the volume of urine excreted.
18.  Diuretics are of limited value when severe renal failure is not severe,
diuretic therapy (usually furosemide {lasix} is helpful if significant edema and
fluid overload are present.  Rarely, children with AGN develop ARF with
oliguria that significantly alters the fluid and electrolyte balance.  Fluid
restriction is needed in case of acute renal failure when urine output is diminished.
19. Hypertension:  Acute hypertension must be anticipated and identified early.
 Blood pressure measurements are taken every 4 to 6 hrs.  Significant but not
severe hypertension is controlled with loop diuretics.  Other antihypertensive
drugs, such as calcium channel blockers, beta blockers, or angiotensin – converting
enzyme inhibitors, may be needed in severe cases. Dialysis:  May be required in
patient with severe and prolonged oliguria or anuria,and renal failure.
20. Penicillin:  Administered of antibiotic (preferably Penicillin) is needed for 7
to 10 days to eradicate streptococci in the throat or skin.  Anti hypertensive
(nifedipine, atenolol) and diuretics are used to control hypertension and its
consequences.  Magnesium sulphate may be prescribed in the encephalopathy to
reduce cerebral edema.  Sedatives (diazepam) may be required in restless
patients.  Management of complication like CCF, hypertensive encephalopathy,
etc should be done promptly to prevent life threatening outcome. Dopamine
infusion, steroid therapy and respiratory support may require for some patients.
21.  Impaired urinary elimination related to glomerular dysfunction.  Infection
related to group A beta- haemolytic streptococcus pharyngitis, upper respiratory
infection.  Fluid volume excess related to altered renal function (or) diminished
glomerular filtration increased Na+ retention.  Activity intolerance related to
edema.  Altered skin integrity related to edema  Altered nutritional, less than
body requirement, related to albuminuria and GI disturbances.  Fear and anxiety
related to disease processes.  High risk for seizure activity related to
hypertensive encephalopathy.  Knowledge deficit regarding care of the child
with renal disease and continuation of care at home.
22. 1.Hypertensive encephalopathy: Manifestations:  Restlessness 
Convulsions  Vomiting  Severe headache  Visual disturbance  Cause –
probably ischemia secondary to vasospasm. Duration:  Usually one to two days.
 Ends spontaneously with decreased blood pressure. 2.Congestive heart failure:
 Cardiac failure may occur due to persistent hypertension, hypervolemia and
peripheral vasoconstriction.
23. Manifestation:  Dyspnoea  Tachycardia  Liver engorgement. Duration:
 Variable  Usually subsides rapidly with the onset the fall in blood pressure.
3.Uraemia (rare): Manifestation:  Evidence of acidosis
24.  Drowsiness  Coma  Muscular twitching  Convulsions. 4.Anaemia:
usually caused by hyperyolaemia rather than a loss of red blood cells in the urine.
5.Renal failure may occur with severe oliguria or anuria or increased B.P  It may
occur in two phases:-  First phase: this stage of edema with oliguria may last for
5 – 10 days.  Second phase: this stage of dieresis starts with the increased of
urine and decreased edema.
25.  Hydronephrosis is a condition in which one or both of the kidneys become
stretched and swollen. This is usually because: There is a blockage somewhere in
the urinary system which is the usual cause, or urine is flowing from the bladder
back to the kidneys  It can sometimes cause a pain in the side, or there may be
no symptoms at all.
26.  Hydronephrosis is distension and dilation of the renal pelvis and calyces,
usually caused by obstruction of the free flow of urine from the kidney, leading to
progressive atrophy of the kidney.
27.  The signs and symptoms of Hydronephrosis depend upon whether the
obstruction is acute or chronic, partial or complete, unilateral or bilateral.
Unilateral Hydronephrosis may occur without any symptoms.  Asymptomatic
(in some cases)  Pain is felt in the renal area  Hematuria  Urinary infection,
dysuria frequency  Renal calculi  Azotemia  Some large Hydronephrosis
can be palpable
28.  History collection  Physical examination: An enlarged kidney may be
palpable on examination. Suprapubic tenderness along with a palpable bladder is
strongly suggestive of acute urinary retention  Blood tests can show raised
Creatinine and electrolyte imbalance.  Urinalysis may show an elevated pH due
to the secondary destruction of nephrons within the affected kidney.  Ultrasound
allows for visualization of the ureters and kidneys and can be used to assess the
presence of Hydronephrosis .
29.  IVU (intravenous urogram) is useful for assessing the position of the
obstruction.  CT 99% of stones are visible on CT and therefore CT is becoming
a common choice of initial investigation.
30. MEDICAL MANAGEMENT Treatment of Hydronephrosis focuses upon 
The removal of the obstruction  Drainage of the urine that has accumulated
behind the obstruction.  The antibiotics are used to prevent the Hydronephrosis
from causing kidney infections.
31. Nephrostomy  Acute obstruction of the upper urinary tract is usually treated
by the insertion of a Nephrostomy (an artificial opening created between the
kidney and the skin which allows for the drainage of urine directly from the upper
part of the urinary system) tube. Ureteric Stent  Chronic upper urinary tract
obstruction is treated by the insertion of a Ureteric stent (a thin tube inserted into
the ureter to prevent or treat obstruction of the urine flow from the kidney)
32. Nephrostomy Ureteric Stent
33. Pyeloplasty  Pyeloplasty is the surgical reconstruction of the renal pelvis to
drain and decompress the kidney. Most commonly it is performed to treat an
uretero-pelvic junction obstruction if residual renal function is adequate.
Suprapubic Catheter  Lower urinary tract obstruction is usually treated by
insertion of a urinary catheter or a suprapubic catheter. Fetal surgery for congenital
Hydronephrosis.  Fetal surgical treatment is done for the correction of posterior
urethral valve obstruction and ureteropelvic junction obstruction.
34. Pyeloplasty Suprapubic Catheter
35. ASSESSMENT History  Elicit a careful history about urinary patterns to
determine a history of burning sensations, abnormal color, and frequency of
urination.  Determine any recent history of mild or severe renal or flank pain that
radiates to the groin.  Ask about vomiting, nausea, or abdominal fullness. Ask a
male patient if he has had prostate difficulties and urinary difficulties. Physical
Examination  Inspect the flank area for asymmetry, which indicates the presence
of a renal mass.  Inspect the male urethra for stenosis, injury, or phimosis.
36.  Inspect and palpate for vaginal, uterine, and rectal lesions in females. When
the flank area is palpated, you may feel a large fluctuating soft mass in the kidney
area that represents the collection of urine in the renal pelvis.  Palpate the
abdomen to help identify tender areas.  If the Hydronephrosis is the result of
bladder obstruction, markedly distended urinary bladder may be felt.  Gentle
pressure on the urinary bladder may result in leaking urine from the urethra
because of bladder overflow.
37. PRE-OPERATIVE NURSING DIAGNOSIS  Hyperthermia related to
infectious process.  Impaired nutritional status less than body requirement
related to hospitalization.  Disturbed elimination pattern incontinence of urine
and related to retention of urine  Deficient knowledge of parents related to the
plan of treatment, surgical procedure and prevention of complications. 
Disturbed family process related to hospitalization of the child.  High risk for
urinary tract infection related to presence of urinary obstruction.
38. POST-OPERATIVE NURSING DIAGNOSIS  Ineffective airway clearance
related to effects of anesthesia, and pain  Acute pain related to incision, and the
surgical procedure  Impaired physical mobility of the upper extremities related
to surgery  Risk for imbalanced fluid volume related to the surgical procedure 
Deficient knowledge of home care procedures  Risk for infection related to the
presence of surgical wound.
39.  Teach the importance of adequate fluids.  Explain the importance of
notifying the physician at the first signs of inability to void or of urinary infection,
such as burning or painful urination, cloudy urine, rusty or smoky urine, blood-
tinged urine, foul odor, flank pain, or fever.
40.  Early detection and prompt treatment has good prognosis. Left untreated,
bilateral obstruction (occurring to both kidneys rather than one) has a poor
prognosis.
41.  Text book of pediatric nursing, editors by “wong and whaley’s”, published
by “n.r.broyhers”, 4th edition, page no:1242-1246.  Dorothy r. marlow, “text
book of pediatric nursing” 6th edition, published by elsevien, page no: 284-290. 
Text book of “essential pediatric nursing”, editors by “piyush gupta”, published by
“a.p. jain and co”, 1st edition, page no: 300- 301.  The short text book of
“pediatric nursing”, editors by “suraj gupte”, published by “jaypee brothers”, 10th
edition, page no: 433-434.
42.  A text book of pediatric nursing, editor by “parul datta”, published by “
jaypee”, 2nd edition, page no: 362-364  The lippincott manual of pediatric
nursing, editor by “barbara f. weller”, published by “chapman and hall”, 8th
edition, page no: 777-778.  Nursing care plans for newborns and children, editor
by “ micheke knoll puzas”, published by “ mosby”, page no: 355 – 357. 
Assuma beevi.t.m., “text book of pediatric nursing”, published by elsevien, page
no: 307-308
Glomerulonephritis (1)
1. PRESENTED BY DR SHASHANK AGRAWAL (MEDICINE)
2.  Glomerular disease includes glomerulonephritis, i.e. inflammation of the
glomeruli and glomerulopathies when there is no evidence of inflammation. 
Glomerulonephritis is a subset of glomerulopathies
3.  Nephrotic syndrome.  Acute glomerulonephritis (acute nephritic
syndrome).  Rapidly progressive glomerulonephritis.  Asymptomatic urinary
abnormality (haematuria, proteinuria or both).
4. Primary – confined to the kidney Secondary – due to a systemic disease
5. 5  Proteinuria – asymptomatic  Haematuria – asymptomatic 
Hypertension  Nephrotic syndrome  Nephritic syndrome  Acute renal
failure  Rapidly progressive renal failure  End stage renal failure
6. 6  Presence of glomerular disease as opposed to tubulointersititial or vascular
disease is suspected from history  Haematuria (especially dysmorphic red cells)
 Red cell casts  Lipiduria (glomerular permeability must be increased to allow
the filtration of large lipoproteins)  Proteinuria (may be in nephrotic range of
>3.5 g/24hours)
7. Immune complex disease  Neutrophils: Protease GBM degradation O₂ free
readicals cell damage AA metabolites ↓ GFR Complement-
dependentComplement-leukocyte- mediated mechanism  Activation of the
complement pathway Recruitment of neutrophils and monocytes C₅- C₉ (MAC)
Epithelial cell detachment.  (+) epithelial & mesangial cells to secrete
damaging chemical mediators. Up regulates TGF receptors on epithelial cells,
excessive synthesis of extracellular matrix which leads to GBM thickening
8.  Named according to  etiology  microscopic findings  clinical
syndrome  Most common clinical presentations  acute nephritic syndrome 
nephrotic syndrome  Most common cause is autoimmune
9.  Autoimmune injury initiated by beta-hemolytic streptococcus  aka acute
proliferative glomerulonephritis  Presents as acute nephritic syndrome 
hematuria  HT  increased urea & creatinine  low urine output  edema 
Antibodies produced by strep throat deposit in glomerulus  Most fully recover
but about 10% evolve into rapidly progressive glomerulonephritis
10.  Unknown causes or secondary to poststreptococcal glomerulonephritis 
Autoimmune  aka crescentric glomerulonephritis  Some present as acute
nephritic syndrome & others as renal failure  Caused by deposition of An-Ab
complexes  All but a few progress to renal failure
11.  Autoimmune  Most common cause of nephrotic syndrome in adults 
About 10% proceed to renal failure within 10 yrs, 25% recover completely, most
progress slowly with proteinuria, HTN, loss of renal function
12.  Incidental discovery of occult proteinuria or HTN  Usually presents as
chronic renal failure or occult proteinuria  Glomerulus has scar tissue 
Dialysis & transplant
13.  Diabetes most common cause  most common cause of renal failure 
glycoproteins deposit in basement membrane  Vascular disease 
atherosclerosis  HTN  vascultitis
14. Heavy proteinuria Proteinuria & haematuria Predominant haematuria Minimal
Change Lupus nephritis Acute post strep Focal sclerosis Membranous Diabetes
Mellitus Amyloidosis Membrano- proliferative Endocarditis Henoch-Schonlein
purpura Crescentic (RPGN) Haemolytic uraemic syndrome
15. 
Acute glomerulonephritis is the inflammation of the glomeruli which causes the
kidneys to malfunction
 It is also called Acute Nephritis, Glomerulonephritis and Post-Streptococcal
Glomerulonephritis
 Predominantly affects children from ages 2 to 12
 Incubation period is 2 to 3 weeks
16.  Infectious
 Streptococcal
 Nonstreptococcal postinfectious glomerulonephritis
▪ Bacterial
▪ Viral
▪ Parasitic
 Noninfectious
 Multisystem systemic diseases
 Primary glomerular diseases
17. Previously M-protein of the organism was felt to be responsible for PSGN.
Recently, nephritis-associated streptococcal cationic protease and its zymogen
precursor (NAPR) has been identified as a glyceraldehyde-3-phosphate
dehydrogenase that functions as a plasmin(ogen) receptor.
18. Diffuse proliferative GN (PGN)  proliferation of cells within the glomeruli,
accompanied by leukocyte filtrate  typical features of immune complex disease :
- hypocomplimentemia - granular deposits of IgG & complement on GBM 
Implicated antigens seem to be endostreptosin and nephritis – plasmin- binding ptn
19.
 Fever
 Headache
 Malaise
 Anorexia
 Nausea and vomiting
 High blood pressure
 Pallor due to edema and/or anemia
 Confusion
 Lethargy
 Loss of muscle tissue
 Enlargement of the liver
20.  Hematuria:
dark brown or smoky urine
 Oliguria: urine output is < 400 ml/day
 Edema: starts in the eye lids and face then the lower and upper limbs then
becomes generalized; may be migratory
 Hypertension: usually mild to moderate
21.  urinary (haematuria, proteinuria),
 nephritic (edemas, hypertension, gross haematuria, proteinuria),
 nephrotic (edemas, proteinuria, hypoproteinemia, hypercholesterolemia),
 mixed.
22.  Abrupt onset of:
glomerular haematuria (RBC casts or dysmorphic RBC).
non-nephrotic range proteinuria (<2 g in 24 hrs).
oedema (periorbital, sacral).
hypertension.
transient renal impairment (oliguria, uraemia).
23. Base line measurements: - ↑ Urea - ↑ Creatinine Urinalysis (MSU): a) Urine
microscopy (red cell cast) b) proteinuria COMPLICATION Hypertensive
encephalopathy, heart failure and acute pulmonary edema may occur in severe
cases Acute renal necrosis due to injury of capillary or capillary thrombosis
24. Treat the underlying infections when acute GN is associated with chronic
infections.  Antimicrobial therapy  Antibiotics (eg, penicillin) are used to
control local symptoms and to prevent spread of infection to close contacts. 
Antimicrobial therapy does not appear to prevent the development of GN, except if
given within the first 36 hours.  Loop diuretic therapy  Loop diuretics may be
required in patients who are edematous and hypertensive in order to remove excess
fluid and to correct hypertension.  Relieves edema and controls volume, thereby
helping to control volume-related elevation in BP.  Vasodilator drugs (eg,
nitroprusside, nifedipine, hydralazine, diazoxide) may be used if severe
hypertension or encephalopathy is present  Diet:  Sodium and fluid restriction
 Protein restriction for azotemic patients  Activity: Recommend bed rest until
signs of glomerular inflammation and circulatory congestion subside.
25. Post streptococcal GN - Has a GOOD prognosis. - Supportive measures until
spontaneous recovery. - Control HT. - Fluid balance. - Oliguric with fluid
overload. - GN complicating SLE or systemic vasculitides: immunosuppression
with prednisolone, cyclophosphamide or azathioprine/MMF.
26. The condition is characterized by irreversible and progressive glomerular and
tubulointerstitial fibrosis. -> ultimately leading to a reduction in the glomerular
filtration rate (GFR) and retention of uremic toxins. -> If disease progression is not
halted with therapy, the net result is chronic kidney disease (CKD), end-stage renal
disease (ESRD), and cardiovascular disease
27. Nearly all forms of acute glomerulonephritis have a tendency to progress to
chronic glomerulonephritis. The progression from acute glomerulonephritis to
chronic glomerulonephritis is variable. Whereas complete recovery of renal
function is the rule for patients with poststreptococcal glomerulonephritis, several
other glomerulonephritides, such as immunoglobulin A (IgA) nephropathy, often
have a relatively benign course and many do not progress to ESRD.
28. Reduction in nephron mass from the initial injury reduces the GFR. This
reduction leads to hypertrophy and hyperfiltration of the remaining nephrons and
to the initiation of intraglomerular hypertension. These changes occur in order to
increase the GFR of the remaining nephrons, thus minimizing the functional
consequences of nephron loss. The changes, however, are ultimately detrimental
because they lead to glomerulosclerosis and further nephron loss.
29. fusion of podocytes on electron microscopy
30. Segmental areas of glomerular sclerosis, hyalinization of glomerular capillaries
31. large glomeruli with mesangial proliferation and ‘double’ BM. 2 histological
types: type I (subendothelial deposits) type II (intramembranous deposits)
32. thickened BM, IF +ve for IgG & C3 and subepithelial deposits on EM
33. Hypercellularity, mesangial proliferation, inflammatory cell infiltrate, positive
IF for IgG and C3 and subepithelial deposits on EM.
34.  Most common cause of GN in Asia but uncommon in Sth America or Africa
 15-40% of all biopsy proven GN  Male > Females  2nd -3rd decade 
Most commonly asymptomatic with serendipitous finding of haematuria and mild
proteinuria  Another classic presentation is macroscopic haematuria in
conjunction with a viral infection  Renal function is usually normal but
occasionally a patient will present with acute renal failure due to acute tubular
necrosis secondary to the gross haematuria  Biopsy – mild to moderate
mesangial cell proliferation, IgA deposits in the mesangium on
immunofluorescence, often with C3 deposition also
35.  Slowly progressive  By 20 years, 50% have end stage kidney disease 
Worse prognosis if >1g/day proteinuria, hypertension, increased creatinine of
glomerular fibrosis at biopsy, on presentation
36.  Uremia-specific findings  Edemas  Hypertension  Jugular venous
distension (if severe volume overload is present)  Pulmonary rales (if pulmonary
edema is present)  Pericardial friction rub in pericarditis  Tenderness in the
epigastric region or blood in the stool (possible indicators for uremic gastritis or
enteropathy)  Decreased sensation and asterixis (indicators for advanced uremia)
37.  Latent (changes in urine)  Hypertensive (increased blood pressure) 
Hematuric  Nephrotic (edemas, proteinuria, hypoproteinemia,
hypercholesterolemia),  Mixed
38.  Urinalysis  Urinary protein excretion  Serum chemistry  Serum
creatinine and urea nitrogen levels are elevated.  Impaired excretion of
potassium, free water, and acid results in hyperkalemia, hyponatremia, and low
serum bicarbonate levels, respectively.  Impaired vitamin D-3 production results
in hypocalcemia, hyperphosphatemia, and high levels of parathyroid hormone. 
Low serum albumin levels may be present if uremia interferes with nutrition or if
the patient is nephrotic.
39.  Renal ultrasonogram  Obtain a renal ultrasonogram to determine renal
size, to assess for the presence of both kidneys, and to exclude structural lesions
that may be responsible for azotemia.  Small kidneys often indicate an
irreversible process.  Kidney biopsy
40.  The target pressure for patients with proteinuria greater than 1 g/d is less
than 125/75 mm Hg; for patients with proteinuria less than 1 g/d, the target
pressure is less than 130/80 mm Hg.  Angiotensin-converting enzyme inhibitors
(ACEIs)  angiotensin II receptor blockers (ARBs)  combination therapy with
ACEIs and ARBs.  Diuretics  Beta-blockers,  calcium channel blockers, 
central alpha-2 agonists (eg, clonidine),  alpha-1 antagonists  direct
vasodilators (eg, minoxidil, nitrates) may be used to achieve the target pressure.
41.  Renal osteodystrophy can be managed early by replacing vitamin D and by
administering phosphate binders.  Seek and treat nonuremic causes of anemia,
such as iron deficiency, before instituting therapy with erythropoietin.  Discuss
options for renal replacement therapy (eg, hemodialysis, peritoneal dialysis, renal
transplantation).  Treat hyperlipidemia (if present)  Expose patients to
educational programs for early rehabilitation from dialysis or transplantation.
42. Minimal change glomerulonephritis (MCGN) Corticosteroids induce remission
in >90% of children and 80% of adults (slower response). Indications for
immunosuppression: (cyclophosphamide, ciclosporin (=cylosporin)): early/
frequent relapses; steroid SEs/dependence. Prognosis: 1% progress to ESRF.
43. Focal segmental glomerulosclerosis Poor response to corticosteroids (10–30%).
Cyclophosphamide or ciclosporin (=cylosporin) may be used in steroid-resistant
cases. Prognosis: 30–50% progress to ESRF.
44. Mesangiocapillary GN Treatment: None is of proven benefit. Prognosis: 50%
develop ESRF.
45. Membranous nephropathy If renal function deteriorates, consider
corticosteroids and chlorambucil. Prognosis: Untreated, 15% complete remission,
9% ESRF at 2–5yrs and 41% at 15yrs.
46. Mesangial proliferative GN Antibiotics, diuretics, and antihypertensives as
necessary. Dialysis is rarely required. Prognosis: Good.
47.  Management  Aggressive control of blood pressure and proteinuria with
ACEI’s or AR2B’s  Corticosteroids +/- azathiprine – varied schools of thought
 However if rapidly progressive GN with crescent deposition treatment should
be aggressive with high dose steroids and cyclophosphamide  Consult the
Nephrologist
48. Rapidly progressive glomerulonephritis (RPGN) is a disease of the kidney that
results in a rapid decrease in the glomerular filtration rate of at least 50% over a
short period, from a few days to 3 months.
49. 50  Classic – haemoptysis after upper respiratory infection and have
nephritic urinary sediment  History of smoking or hydrocarbon exposure is
common  CXR – pulmonary haemorrhage  Lab- iron deficiency anaemia and
renal dysfunction, circulating anti-GBM antibodies  Kidney biopsy crescentic
GN with linear staining IgG and C3 along the glomerular basement membrane
50. More than 80% of patients with pauci-immune RPGN were subsequently found
to have circulating antineutrophil cytoplasmic antibodies (ANCA), and thus, this
form of RPGN is now termed ANCA-associated vasculitis.
51. RPGN is classified pathologically into 3 categories:  (1) anti-GBM antibody
disease (approximately 3% of cases),  (2) immune complex disease (45% of
cases),  (3) pauci-immune disease (50% of cases).
52.  Symptoms and signs of renal failure,  pain,  haematuria,  systemic
symptoms (fever, malaise, myalgia, weight loss).
53.  The most important requirement in the diagnosis of antineutrophil
cytoplasmic antibodies (ANCA) ANCA-associated disease is a high index of
suspicion. Rapid diagnosis is essential for organ preservation. Laboratory studies
include the following:  Routine chemistry: The most common abnormality is an
increased serum creatinine level.  Urinalysis with microscopy:  Antinuclear
antibody (ANA) titer:  ANCA .
54. High-dose corticosteroids; cyclophosphamide ± plasma exchange/ renal
transplantation. Prognosis: Poor if initial serum creatinine >600µmol/L.
55. THANK YOU
Glomerulonephritis
1. Glomerulonephritis<br />Matthew Patjawee<br />
2. Overview
Glomerulonephritis: glomeruli kidney inflammation<br />Alternative names:
acute/chronic nephritis, glomerular disease<br />
Definition: Type of kidney disease in which the part of the kidneys that help filter
waste and fluids from the blood is damaged. Damage to the glomeruli causes blood
and protein to be lost in the urine.
3. Glomeruli
Glomeruli – The filters of the kidneys which filter the blood and make urine.
4. Etiology
Often, the precise cause of glomerulonephritis is unknown.Glomerulonephritis
may be caused by specific problems with the body's immune system.
5. Signs/Symptoms<br />
Most common symptoms:
 Hematuria (dark, brown, or rusty colored,)
 Proteinuria
 Foamy urine
 Swelling of the face, eyes, ankle, feet, legs, abdomen
6. Signs/Symptoms
Symptoms which may also appear include:
 Abdominal pain
 Cough
 Diarrhea
 Fever
 Joint aches
  Muscle aches
 Loss of appetite
 Shortness of breath
7. Risk Factors
 History of cancer
 Blood or lymphatic disorders
 Exposure to hydrocarbon solvents
 Diabetes
 Infections
 Strep infections
 Heart infections
 Viruses
8. Diagnosis
Because symptoms develop gradually, the disorder may be discovered when there
is an abnormal urinalysis during a routine physical or examination for unrelated
disorders.
9. Tests and Clinical Procedures
 Imaging tests:
 Abdominal CT scan
 Abdominal ultrasound
 Chest x-ray
 Intravenous Pyelogram (IVP)
Urinalysis and other urine tests:
 Creatinine clearance
 Urine concentration test
 Urine specific gravity
 Total protein
10. Treatments<br />
Treatment varies depending the type and severity of symptoms. <br />
High blood pressure may be difficult to control, and it is generally the most
important aspect of treatment.<br />
Medicines that may be prescribed include:<br />
Blood pressure medications are often needed to control high blood pressure. <br />
Medications that suppress the immune system may also be prescribed, depending
on the cause of the condition.<br />
11. Prognosis<br />
Glomerulonephritis may be a temporary and reversible condition, or it may get
worse. Progressive glomerulonephritis may lead to chronic kidney failure and end-
stage kidney disease.<br />
12. Case Study<br />Patient: <br />12 year old girl who visited the doctor in
distress.<br />Symptoms:<br />Has been passing rusty colored urine.<br />Looked
puffy around the face.<br />High blood pressure.<br />Doctor saw previous
antibiotics given for streptococcal infection in her records.<br />Doctor used test
strip to test urine.<br />Resulted in presence of protein.<br />Blood test was
arranged<br />Blood test suggested an autoimmune response had damaged part of
the kidneys nephrons.<br />Doctor suggested she be closely watched for the time
being and blood pressure monitored.<br />Her condition fortunately cleared up
after a few months.<br />

Nephrotic syndrome- B.Sc. Nursing III yr

1. Presentation on nephrotic syndrome SUBMITTED BY:- Rahul Dhaker , Asst.
Professor, PCNMS, Nainital 1
2. INTRODUCTION  The nephrotic syndrome is a clinical state characterized
 proteinuria ,  hypoalbuminemia ,  hyperlipidimia and  edema sometimes
accompanied by hematuria, hypertension and reduced glomerular filtration rate. 2
3. DEFINITION Nephrotic syndrome is a group of symptoms that include protein
in the urine , low blood protein levels in the blood, high cholesterol levels , high
cholesterol levels, high triglyceride levels, and swelling. 3
4. INCIDENCE Nephrotic syndrome is common among children in the age of 2-6
years. Mean age of onset is 2.5 years. It is more common in males than in females.
4
5. ETIOLOGY • Nephrotic syndrome has many causes and many either be result
of a disease limited to kidney called primary nephrotic syndrome or a condition
that affects the kidney and other part of the body called secondary nephrotic
syndrome. 90% of the cause in idiopathic. 5
6. PRIMARY GLOMERULONEPHROSIS Primary causes of nephrotic syndrome
are usually described by their history. Minimal change disease Focal
segmental glomerulosclerosis Membranous proliferative glomerolonephritis
(MPGN) Membranous glomerulonephritis (MGN) Rapidly progressive
glomerulonephritis 6
7. SECONDARY GLOMERULONEPHROSIS Secondary causes of nephrotic
syndrome have the same histological patterns as the primary causes though they
may exhibit same different a suggesting a secondary cause, such a inclusion
bodies. Diabetic nephropathy Systemic lupus erythermatous Sacroidosis
Syphilis Hepatitis B HIV 7
8. • Amyloidosis • Multi myeloma • Vasculitis • Genetic disorder • Drug 8
9. CLINICAL MANIFESTATION The onset is slow, features of nephrotic
syndrome include: Puffing around the eyes characteristically in the morning.
Pitting edema over the legs Fluid in the pleural cavity causing pleural
effusion. More excess fluid is pulmonary edema. Generalized edema Ascites
9
10. • Hydrothorax and hydrocele • Hematuria • Fever , rash and joint pain • Pallor •
Irritability • Loss of appetite but weight gain 10
11. 11
12. DIAGNOSTIC EVALUATION  URINE ANALYSIS:-  24 hr urinary
total protein estimation- urine sample show proteinuria(>3.5gper liter per 24hrs) it
is also examined for casts, which are more a feature of active nephritis . 
Comprehensive metabolic panel shows hypoalbuminiemia albumin level is < 2.5
g/dl(normal level is 3.5-5g/dl)  Lipid profile show high level of cholesterol . 12
13. BLOOD:- Blood total serum albumin- reduced Serum albumin- reduced
Serum globulin-normal or increased Cholesterol- increased RENAL
ULTRASOUND:- RENAL BIOPSY- for histology examination of renal tissue
to confirm the diagnosis. 13
14. 14
15. 15
16. MANAGEMENT The objectives of treatment are: 1. Control of infection 2.
Normal adjustment of the disturb process 3. Control of edema 4. Promotion of
good nutrition 5. Promotion of good physical and mental hygiene. 16
17. MEDICAL MANAGMENT Corticosteroid therapy  prednisolone is the
drug of choice. Daily dose of 2mg/kg/day orally in divided doses 6 week is given,
thereafter 1.5mg/kg as single dose an alternate days. For 6weeks after which
treatment is discontinued. Frequent relapses are treated by alkylating agents such
as cyclophoshamide( 2mg/kg daily for 12 week) nitrogen , mustard cyclosporine or
levamisole . 17
18. • Diuretic and salt albumin may be indicated in presence of severe edema.
Frusemide (1- 44mg/kg/day in 2 divided doses) alone or with aldosterone
antagonist spiroholactone (2- 3mg/kg/day in 2 divided doses) may be prescribed.
18
19. NURSING MANAGEMENT 1. Impaired urinary elimination related to Na and
water retention. 2. Excess fluid volume related to edema. 3. Imbalance nutrition
less than body requirement related to damage metabolism. 4. Anxiety related
hospitalization of child and caring for child with a chronic disease. 19
20. SURGICAL MANAGEMENT:- Renal transplant 20
21. COMPLICATION: Acute renal failure, renal vein thrombosis.
Atherosclerosis and related heart disease . Chronic kidney disease. Fluid
overload, congestive heart failure, pulmonary edema. Infection including
pneumococcal pneumonia 21
22. BIBLIOGRAPHY • Sharma Rimple essential of pediatric nursing published
by- Jaypee brothers medical publishers(P) Edition- first edition , Page no- 465-470.
• Singh& Jacob pediatric nursing published by – N.R brothers Edition –fourth
edition 2009, page no-318-322. • Ghai OP Essential pediatric published by- CBS
publishers & distributors edition- 450- 454. 22

Nephrotic syndrome
1. NEPHROTIC SYNDROME PREPARED BY: MANISHA PRAHARAJ MSC.
NURSING 2ND YEAR
2. DEFINITION Nephrotic syndrome is a primary glomerular disease
characterized by proteinuria, hypoproteinemic edema and hypercholesterolemia
hypoalbuminemia, hyperlipidemia. Because of gross proteinuria serum albumin is
low ( <2.5 g/dl).
3. TYPES 1. Idiopathic NS: In childhood, the vast majority belongs to category it
is regarded as a sort of autoimmune phenomenon, especially since it responds well
to immunosuppressive therapy. It is two types: a. Minimal change NS – this
predominant type, seen 86% of the cases. b. Significant change NS – this is
infrequent. Mesangial proliferation is seen in 5% cases and focal sclerosis in 10%
of cases.
4. 2. Secondary NS: • It occurs in children (about 10%) of all cases. • This
condition may occur due to some form of chronic glomerulonephritis, or due to
diabetes mellitus, SLE, malaria, malignant hypertension, hepatitis B, infective
endocarditic, HIV/AIDS, drug toxicity, lymphomas syphilis etc.
5. 3. Congenital NS: • It is rare but a serious and fetal problem usually associated
with other congenital anomalies of kidney. • It is inherited as autosomal recessive
disease. • Severe renal insufficiency & urinary infections along with this condition
result is poor prognosis.
6. 4. Infantile NS: • The term is applied to NS occurring in infants between 4 –
12months of age. Its major causes are: A. NPHS2 B. Diffuse mesengial sclerosis
(DMS)
7. ETIOLOGY 1. Primary renal cause • Minimal change nephropathy •
Glomerulosclerosis • Acute post streptococcal glomerulonephritis • Immune
complex glomerulonephritis.
8. 2. Systemic cause • Infections • Toxins – mercury, bismuth, gold • Allergic –
bee sting, inhaled pollen, food allergy • Cardiovascular – sickle cell disease, renal
vein thrombosis, congestive heart failure • Malignancies – leukemia • Others –
systemic lupus erythematous, anaphylactic purpura
9. PATHOPHYSIOLOGY Alteration in glomerular basement membrane
Decreased colloidal osmotic pressure Decreased vascular volume Decreased renal
blood flow Increased loss of protein in urine Altered glomerular protein
permeability Increased secretion of aldosterone Edema Tubular Na and H2O
reabsorption
10. CLINICAL MANIFESTATION Four main symptoms of nephritic symptoms:-
• Protein urea • Hypoalbuminemia • Hyperlipidemia • Edema
11. OTHERS: • SOB (Shortness of breath) • Mild headache • Fever, rash, joint
pain • Weakness • Malaise • Anorexia • Weight gain • Periorbital edema •
Irritability • Ascites • HTN • Anemia due to loss of RBCs • Flank pain • Fatigue.
12. DIAGNOSIS o PALPATION: Due to edema and ascites kidney cannot be
palpable. o Urine analysis Haematuria 24 hour urinary total protein estimation –
urine sample shows proteinuria (>3.5 g per liter per 24 hours) o Blood test BUN
S.creatinine S.protein Desreases Lipid profile shows high level of S. cholesterol-
200mg.
13. • Comprehensive metabolic panel(CMP) shows hypoalbuminemia, albumin
level is <2.5g/dl  Needle biopsy of kidney  ECG  KUB – X.ray  Renal
ultrasound  Renal scan  Intravenous urogram (IVU).
14. MANAGEMENT MEDICAL MANAGEMENT: • The goal of medical
management is reduction of protein excretion. • If causative agent is streptococcal
then treated with penicillin antibiotics. • Prednisolone is the drug of choice. Daily
dose of 2mg/kg/day orally in divided doses for 6 weeks is given, • Thereafter 1.5
mg/kg as single dose on alternate days for 6 weeks, after which treatment is
discontinued.
15. • Proteinuria disappears within the first week of therapy and negative dipstick
test for 2 consecutive days shows positive response to treatment. • Frequent
relapses are treated by alkylating agents such as cyclophosphamide (2 mg/kg daily
for 12 weeks), nitrogen mustard, cyclosporine or levamisole. • Diuretic and salt
poor albumin may be indicated in presence of severe edema. • Frusamide (1-44
mg/kg/day in 2 divided doses) may be prescribed.
16. DIETARY MANAGEMENT • Children should take a well-balanced diet rich
in protein. Sodium is restricted when marked edema is present. • Provide high
protein and high carbohydrates diet to patient. • If disease in advance stage then
avoid protein intake because it is affected to kidney. • Water restriction may be
indicated if decreasing salt intake does not control edema.
17. NURSING MANAGEMENT NURSING DIAGNOSIS: • Risk for infection
related to immunosuppressive drugs. • Fluid and electrolyte imbalanced related to
edema. • Impaired skin integrity related to disease process. • Altered nutrition
related to Anorexia. • Altered kidney function related to disease condition. •
Knowledge deficit related to disease process.
18. Care during hospitalization: • Child is hospitalized from initial therapy. Patient
may not understand importance of hospitalization because initially the child is
symptomless. During hospitalization parents should be involved in child care and
goal setting. • Nurses should regularly monitor the vital signs and check the Childs
daily weight.
19. • Monitor signs of infection and edema. • Detailed chatting of intake/output
most be done to monitor child’s response to medical therapy. • Daily urine
examination for albumin is required.
20. B. Administer the prescribed medications: o Children with nephritic syndrome
are receiving steroids so the nurse most be aware of the side effects of these drugs.
Patient should be observed for gastrointestinal bleeding, gastro intestinal ulcers,
hyperglycemia and cataract. o Steroid is continued till the child is protein free,
thereafter the drug dose in decreased gradually.
21. Maintain fluid and electrolyte balance: • Nurses should monitor serum sodium
level of the child. • Fluid intake either oral or I/V should be strictly monitored. •
Child is assessed for venous stasis, ascites and pulmonary edema. • Daily weight of
child is accurately documented.
22. Prevention of infection: • The child is on corticosteroid therapy
(immunosuppressant) and there is loss of immunoglobulin in urine, so these
children are the greater risk of infection. • Strict aseptic technique should be used
during invasive procedures. • Monitor vital signs for early signs of infection. •
Isolate the child as he is on immunosuppressive therapy.
23. Promote rest: • Provide passive play to the child as tolerated e.g, watching TV,
reading story books, etc. • Allow a period of rest after activities. • Limit visitors
during acute phase of illness.
24. Provide emotional support: • Explain parents about the disease and its
treatment • Allow the patients and child to express their feelings. • Due to sudden
weight gain and disturbed body image, child may manifest with behavioral
changes, may refuse to look at mirror and has decreased interest in appearance. •
Enhance the body image of the child. • Encourage child to wear own clothes rather
than hospital clothes as this make the child feel good.
25. Discharge plan • Explain to patients about treatment programmed, follow up
and risk of relapse. • Encourage patients to measure child’s weight weekly in order
to identify early fluid retention. • Tell then to contact doctor if any unusual
symptoms appear. • Increase intake of fruits and vegetables. No potassium and
phosphorus restriction in necessary.
26. o Explain about the medications to be continued at home and their side effects
like cushingoid appearance, gastrointestinal bleeding and sodium retention. If the
child is on corticosteroid therapy for very long time, fundus checkup should be
done because prednisolone causes cataract. o Dietary modifications should be
explained to the parents. o Ask them to avoid saturated fats such as butter, cheese,
fried foods, and fatty cuts of red meat and egg yolks and increase unsaturated fat
intake including olive oil, canola oil, peanut butter, and nuts. The child can eat low
fat desserts.
NEPHROTIC SYNDROME
1. NEPHROTIC SYNDROME By Dr.Raman Kumar
2. DEFINITION PROTEINURIA Nephrotic range HYPOALBUMINEMIA
HYPERLIPIDEMIA OEDEMA
3. Nephrotic Range Proteinuria 24 hour urine..40mg/m2/h…difficult First morning
urine sample…protein and creatinine ratio….more than 2-3:1
4. Classification of nephrotic syndrome ETOLOGICAL CLASSIFICATION
Primary NEPHROTIC syndrome. Disease limited to kidney Secondary
NEPHROTIC syndrome. Other systems involved HISTOLOGICAL
CLASISIFICATION MCD FSGN MN MPGN
5. Causes of secondary nephrotic syndrome <ul><li>Membranous nephropathy
(MN) [3] </li></ul><ul><li>Hepatitis B </li></ul><ul><li>Sjogren's syndrome
</li></ul><ul><li>Systemic lupus erythematosus (SLE)
</li></ul><ul><li>Diabetes mellitus </li></ul><ul><li>Sarcoidosis
</li></ul><ul><li>Syphilis </li></ul><ul><li>Drugs
</li></ul><ul><li>Malignancy (cancer) </li></ul><ul><li>Focal segmental
glomerulosclerosis (FSGS) [3] </li></ul><ul><li>Hypertensive Nephrosclerosis
</li></ul><ul><li>Human immunodeficiency virus (HIV)
</li></ul><ul><li>Diabetes mellitus </li></ul><ul><li>Obesity
</li></ul><ul><li>Kidney loss </li></ul><ul><li>Minimal change disease (MCD)
[3] </li></ul><ul><li>Drugs </li></ul><ul><li>Malignancy, especially Hodgkin's
lymphoma </li></ul>Primary nephrotic syndrome Diagnosis of exclusion
6. Primary nephrotic syndrome /idiopathic nephrotic syndrome Steroid resistant
INS (SRNS) Steroid sensitive IN (SSNS) response to steroids has a high
correlation with histological subtype and prognosis
7. PATHOPHYSIOLOGY PROTEINURIA / HYPOALBUMINIA Immune
pathogenesis Deregulation of T-cell subsets. Circulating factors Cytokines/other
molecules Allergic response Poison ivy, bee stings
8. PODOCYTE BIOLOGY Effacement of podocytes is now thought to be the
primary pathology. -ve charge of the basement membrane is also important.
9. GENETICS. Nephrin Transmembrane protein encoded by NPHS 1 on
chromosome 19.(FINISH type congenital NS. Podicin Encoded by NPHS 2 on
chromosome 1. Autosomal recessive. Mutations in α-actinin-4, encoded by the
gene ACTN4 on chromosome 19 and TRPC6 on chromosome 11, are associated
with autosomal dominant forms of FSGS
10. PATHOPHYSIOLOGY continued….
11. Pathophysiology cont… Decreased plasma oncotic pressure may play a role in
increased hepatic lipoprotein synthesis, as demonstrated by the reduction of
hyperlipidemia in patients with INS receiving either albumin or dextran infusions
Patients with nephrotic syndrome are at increased risk for thrombosis.
Abnormalities described in INS include increased platelet activation and
aggregation; elevation in factors V, VII, VIII, and XIII and fibrinogen; decreased
antithrombin III, proteins C and S, and factors XI and XII; and increased activities
of tissue plasminogen activator and plasminogen activator inhibitor-1. Decreased
levels of Ig G and increased losses of factor B.
13. INVESTIGATIONS ESTABLISH nephrotic syndrome Nephrotic range
proteinuria Hypoalbuminemia Hyperlipidemia Primary or secondary nephrotic
syndromes If Primary, Whether in renal failure?.... Renal functions.
14. Investigations Urea creatinine and electrolytes CBC Testing for hep B and C
Complement system ANA,Anti double stranded DNA antibodies. Imaging;U/S
abdomen and chest. X ray chest. Genetic testing. Renal biopsy
15. INTERPRETATIONS Anemia , raised urea creatinine
,acidosis,hyperkalemia,hyperphosphatemia,indicate Chronic renal disease.
Hyponatremia may be due to hyperlipidemia and due to water
retention(pseudohyponatremia. Raised Hb and haemetocrat indicates
haemodilution.reduced intravascular volume. Platelet is raised. Check liver
enzymes..for Hepatitis B and C.and do screening for viruses.
16. MANAGEMENT OF NEPHROTIC SYNDROME A trial of corticosteroids is
the first step in treatment of idiopathic nephrotic syndrome (INS) in which kidney
biopsy is not initially indicated. patients aged 1-8 years with normal kidney
function Normal kidney functions No macroscopic gross haemeturia No symptoms
of systemic disease. Normal complement levels Negative viral screen No family
hisory.
17. IMPORTANT DEFINITIONS RESPONSE; protein free urine on 3
consecutive days within 7 days. RELAPSE; protein +ve urine on 3 consecutive
days within one week with edema. FREQUENT RELAPSING NS; steroid
sensitive nephrotic syndrome with 2 or more relapses in 6 months or more than 3
in one year. STEROID DEPENDANT; responder who relapses while steroid is
being tapered or within 14 days of stopping steroid treatment.
18. INITIAL NON RESONDER; no response during initial 8 weeks of therapy.
LATE NON RESPONDER; an initial steroid responder who fails to respond to 4
week treatment in relapse.
19. SSNS steroid sensitive nephrotic syndrome Corticosteroids INDUCTION
THERAPY Exclude active infections and other contraindications to steroids Oral
prednisilone 60mg/m2/day…either single or divided doses for 4 weeks. 6 weeks
therapy proves better . MAINTAINANCE THERAPY Oral prednisilone at
40mg/m2/day single morning dose at alternate Days for 4-6 weeks. Longer
duration of maintenance therapy results in fewer relapses.
20. Relapse therapy For infrequent relapses steroid therapy may be resumed at
60mg/m2/day until proteinuria resolves.. Then switch to 40mg/m2/day for alternate
days for 4 weeks. Other therapy Pneumococcal vaccines to all the patients.
Diuretic therapy for symptomatic edema. with furosamide 2mg/kg/day. Anasarca
with low intravascular volume ,albumin infusion, slow 1mg/kg/day can be
considered.
21. HOME MONITORING Home monitoring of urine protein and fluid status is
important. Parents should be trained to monitor first morning urine by dipstick.
Record of daily weight,urine protein and steroid dose should be kept in log book.
Any increase in urine protein or daily weight should be reported as early as
possible.
22. TREATING FREQUENT RELAPSERS AND SDNS ALKYLATING
AGENTS Cyclophospamide Chlorambucil Nitrogen mustard CALCINEURINE
INHIBITORS Cyclosporin Tacrolimus LEVAMISOLE MYCOPHENOLATE
MOFETIL
23. DOSING AND REGIMENS Cyclophosphamide (2–2.5 mg/kg daily) is given
orally for 8-12 weeks. Steroids are usually overlapped with initiation of CYP then
tapered Patients must have weekly CBC counts to monitor for leukopenia. Patients
must also maintain adequate hydration and take CYP in the morning (not at
bedtime) to limit the risk of hemorrhagic cystitis
24. CYCLOSPORIN CSA can be used in those children who fail to respond to, or
subsequently relapse after, treatment with CYP, or for children whose families
object to use of CYP Initial doses of CSA are started at 5–6 mg/kg daily divided
every 12 hours, adjusted for trough concentrations of 50–125 ng/mL Low-dose
steroids are continued for a variable length of time <ul><ul><ul><li>Kidney
function and drug levels must be carefully monitored due to the risk of CSA
induced nephrotoxicity. </li></ul></ul></ul>
25. Deterrence/Prevention Yearly influenza vaccination is recommended to prevent
serious illness in the immunocompromised patient, as well as to prevent this
possible trigger of relapse. Pneumococcal vaccination should be administered to all
patients with INS to reduce the risk of pneumococcal infection. Vaccination should
be repeated every 5 years while the patient continues to have relapses. Routine
childhood vaccines with live virus strains are contraindicated in patients taking
steroids and until off steroid treatment for a minimum of 1 month. Because of the
high risk of varicella infection in the immunocompromised patient, in the
nonimmune patient, post exposure prophylaxis with varicella-zoster immune
globulin is recommended. Patient with varicella-zoster infection should be treated
with acyclovir and carefully monitored Routine, nonlive viral vaccines should be
administered according to their recommended schedules
Nephrotic syndrome By Sachin Dwivedi
1. NEPHROTIC SYNDROME By Mr. Sachin dwivedi M.Sc. (N) Medical surgical
Nursing
2. OUTLINE • Introduction • Anatomy and Physiology of Kidney. • Definition. •
Incidence. • Cause • Pathophysiology. • Clinical Manifestation. • Diagnostic
measure. • Management: Medical, Pharmacological and Nursing. • Complication. •
Prognosis.
3. Genito-Urinary System G.U.S. Kidneys Ureters. Bladder. Urethra.
4. Function of Genito-Urinary System Produce and excrete urine Regulate the
volume Acid –Base balance of body fluid Detoxify the blood and remove waste
Support red cell production.
5. NEPHRON • Nephron: functional unit of kidney. • Glomerulus (rounded
structure of Blood capillaries ). • Glomerular capsule • Proximal convoluted tubule
• Loop of Henle. • The distal convoluted tubule
6. PHYSIOLOGY The urine is formed by certain process:- • Glomerular filtration
• Tubular filtration • Tubular secretion
7. INTRODUCTION Nephrotic/syndrome kidney / A group of symptoms •
Nephrotic syndrome is a collection of symptoms due to kidney damage. • This
includes protein in the urine, low blood albumin levels, high blood lipids, and
significant swelling.
8. DEFINITION • Nephrotic syndrome is a primary glomerular disease
characterized by- 1. Proteinuria 2. Hypoalbuminemia. 3. Hyperlipidemia.
9. INCIDENCE • Nephrotic syndrome is present in as many as 7 children per 100,
000 population younger than 9 years of age. • The average age of onset is 2.5
years, with most cases occurring between the ages of 2 and 6 years.
10. Etiology Nephrotic Syndrome Primary cause Secondary Cause
11. PRIMARY CAUSE OF NEPHROTIC SYNDROME Primary Cause
MINIMAL CHANGE DISEASE MEMBRANE GLOMERULONEPHRITIS
MEMBRANOPROLIFERATIV E GLOMERULONEPHRITIS RAPIDLY
PROGRESSIVE GLOMERULONEPHRITIS FOCAL
GLOMERULOSCLEROSIS
12. SECONDARY CAUSES OF NEPHROTIC SYNDROME Systemic lupus
erythematosus Diabetes mellitus Bacterial infection Drugs: NSAIDs
13. PATHOPHYSIOLOGY LOSS OF PLASMA PROTEIN [ ALBUMIN] DUE
TO CAUSES- DAMAGE GLOMERRULAR CAPILLARY MEMBRANE
STIMULATES SYNTHESIS OF LIPOPROTEIN HYPERLIPIDEMIA
HYPOALBUMINEMIA GENERALIZED OEDEMA ACTIVATION OF RENIN
ANGIOTENSIN SYSTEM SODIUM RETENTION EDEMA DECREASE
OSMOTIC PRESSURE FLUID MOVES FROM IVS TO ECS
14. CLINICAL MANIFESTATION NEPHROTRIC SYNDROME
HYPERLIPIDEMIA HYPO- ALBUMINEMIA PROTEINURIA
15. CLINICAL MANIFESTATION • Generalized edema(anasarca.). • Puffiness
around the eyes&face . • Pitting edema over the arms and legs • Weight gain. •
Haematuria. • Oliguria. • Fever, chills Weakness, lethargy. • Nausea and vomiting.
• Hypertension
16. DIAGNOSTIC MEASURES History Taking: Physical Examination: Blood
test: Elevated electrolyte, BUN, Creatinine, Decrease Hb. Comprehensive
Metabolic Panel: Urinalysis: Protein, Throat Culture: (Group-a Beta H.) KUB:
show bilateral Renal Enlargement
17. Medical Management • Fluid restriction to decrease edema. • Monitor Intake
and output chart • Dietary sodium restriction. • Correction of electrolyte imbalance.
18. Pharmacological Management • Antibiotic therapy: amoxicillin 500 mg/BD •
Loop Diuretic such as Lasix 1-2 mg/kg/d/ IV • ACE Inhibitors and Angiotensin
receptor blocker Such as anapril initial: 2.5-5 mg PO qDay. • Corticosteroids such
as pridnisone 1 mg/kg/day.
19. Nursing Management Nursing Assessment • Assess the complete history of
client. • Assess the signs of edema, pitting and facial puffiness. • Assess fluid
intake and output. • Assess the condition of skin, • Assess the blood pressure,
Respiration, Temperature.
20. Nursing Diagnosis 1. Excess Fluid Volume related to fluid accumulation. 2.
Imbalance nutrition less then body requirement related poor appetite. 3. Activity
Intolerance related to insufficient physiological energy. 4. Risk for impaired skin
integrity related low body defense. 5. Risk for Infection related to
immunosuppression.
21. Nursing Intervention • Monitoring fluid intake and output. • Improving
nutritional intake. • Promoting skin integrity. • Promoting energy conservation. •
Preventing infection.
22. COMPLICATIONS Atherosclerosis. Hypertension. Nutritional deficiency
Renal failure Infection
23. PROGNOSIS • The prognosis depends on the cause of nephrotic syndrome. • It
is usually good in children, because minimal change disease responds very well to
steroids and does not cause chronic renal failure. • However other causes such as
focal segmental glomerulosclerosis frequently lead to end stage renal disease.
24. SUMMARY • Introduction • Anatomy and Physiology of Kidney. • Definition.
• Incidence. • Cause • Pathophysiology. • Clinical Manifestation. • Diagnostic
measure. • Management: Medical, Pharmacological and Nursing. • Complication. •
Prognosis.
25. REFERENCES • Brunner and Suddarth's (2010)Textbook of Medical-Surgical
Nursing, 10th edition, Lippincott Williams & Wilkins,. • Black M.Joyce and
Hawks Hokanson Jane. (2012). Medical Surgical Nursing,Clinical Management for
Positive Outcome.Mumbai.Elsevier Publication. • Black. M. Joyce et.al. (2005).
Medical Surgical Nursing.8th edition .Vol.2 • Hinkle L. Janice and Cheever H.
Kerry (2014).Text book of Medical-Surgical Nursing 13th edition. NewDelhi.
Wolters Kluwer publication. • Nephrotic syndrome, Nurseslabs, retrieved on 05
July 2019 from https://nurseslabs.com/nephrotic-syndrome/. • Nephrotic
syndrome, Kidney Foundation retrieved on 05 July 2019 from
http://www.kidneyfund.org/kidney-disease/other- kidney-conditions/rare-
diseases/nephrotic-syndrome/.
26. THANK YOU
Chronic Renal Failure (End Stage Renal Failure)
1. Mr.Sachin Dwivedi M.SC. Medical surgical Nursing K.G.M.U Institute of
Nursing , Lucknow
2. Chronic kidney Disease
3. Chronic kidney disease (CKD)  Chronic kidney disease (CKD) consists of a
spectrum of different pathophysiologic processes associated with abnormal kidney
function, and a progressive decline in glomerular filtration rate (GFR).
4. Acc. To National kidney foundation, It is defined as………. 1.Kidney damage
for ≥3 months, as defined by structural or functional abnormalities of the kidney,
with or without decreased GFR, manifest by either:  Pathological abnormalities
or  Markers of kidney damage 2. GFR <60ml/min/ for ≥3mths, with or without
kidney damage.
5. Epidemiology  Chronic kidney disease is a growing health problem in the
United States.  A report by the Centers for Disease Control (CDC) determined
that 16.8% of all adults above the age of 20 years may have chronic kidney
disease.  Incidence: 200 cases per 1 million persons U.S.
6. Risk factors  Diabetes mellitus,  Hypertension,  Autoimmune disease, 
Older age,  A family history of renal disease,  A previous episode of acute
renal failure,  Structural abnormalities of the urinary tract.
7. Causes of chronic kidney disease Primary glomerular diseases: 
Glomerulonephritis, IgA nephritis, pyelonephritis. Systemic disease: diabetes
mellitus, hypertension, Postinfectious glomerulonephritis, SLE, Hereditary
nephropathies:  Hereditary nephritis  Polycystic kidney disease
8. Cont… Vascular causes:  Large vessel disease such as bilateral renal artery
stenosis  Small vessel disease such as ischemic nephropathy and vasculitis.
Obstructive causes: such as  bilaterl kidney stones and  diseases of the
prostate,  urinary system tumors,  Vesicoureteral reflux
9. Compensatory hypertrophy of surviving nephrons adaptive hyper filtration &
hypertrophy. Loss of excretory function Loss of non- excretory renal function.
sclerosis of remaining nephrons, & total function loss. Decreased ph, k+,
nitrogenous waste excretion. Like failure to produce erythropoietin & to convert
inactive form of calcium Pathophysiology
10. Classification of Chronic Kidney Disease (CKD) Stage Description GFR,
ml/min 0 With risk factors. >90, 1 Kidney Damage with normal GFR. ≥90, 2
Kidney Damage with mild ↓ in GFR. 60-89 3 Moderate ↓ 30-59 4 Severe ↓in GFR
15-29 5 Kidney failure <15 http://www.kidney.org/
11. Stage 5 CKD is also called established chronic kidney disease and is
synonymous with the now outdated terms  end-stage renal disease (ESRD), 
chronic kidney failure (CKF) or  chronic renal failure (CRF).
12. Chronic renal failure : Applies to the process of continuing significant
irreversible reduction in nephron number, and typically corresponds to CKD stages
3–5.
13. End-stage renal disease  The term represents a stage of CKD where the
accumulation of toxins, fluid, and electrolytes normally excreted by the kidneys
results in the Uremic syndrome.  No more compensation; all other organ systems
will end up with some kind of dysfunction.  This syndrome leads to death unless
the toxins are removed by renal replacement therapy, using dialysis or kidney
transplantation.
14. Clinical manifestations Neurological – Central:  Slurred speech  Asterixis
and myoclonus  Seizures  Disorientation and confusion  Increased muscle
fatigability
15. Clinical manifestations  Failure of kidneys to remove excess fluid may
cause:  Edema of the legs, ankles, feet, face and/or hands  Shortness of breath
due to extra fluid on the lungs (may also be caused by anemia)  hypertension
and/or congestive heart failure
16. Metabolic changes 1.An increase in serum creatinine or BUN. High levels of
urea in the blood, which can result in:  Vomiting and/or diarrhea, which may
lead to dehydration.  Weight loss  Nocturnal urination  Azotemia and
ultimately uremia.
17. Metabolic changes 2. Proteinuria 3.Hyperphosphatemia
18. Metabolic changes 5. Hyperkalemia may cause:  Abnormal heart rhythms
Metabolic acidosis: due to accumulation of sulfates, phosphates, uric acid etc.
19. Hematological changes  Erythropoietin synthesis is decreased leading to
anemia, which causes:  Feeling tired and/or weak  Memory problems 
Difficulty concentrating  Dizziness  Low blood pressure
20. GIT changes  Appetite loss, a bitter, metallic or salty taste in the mouth 
Fishy or ammonia-like smell in breath  Difficulty sleeping  Gastritis, 
constipation
21. Cardiovascular changes  50%-65% deaths occur due to cardiac
complications of CKD.  Hypertention  Left ventricular hypertrophy 
Electrolyte imbalance  Myocardial calcification
22. Respiratory changes  Pulmonary edema  Pleuritis  Tachypnea
23. DIAGNOSIS
24. DIAGNOSIS 1.Urine tests: a) Urinalysis: dipstick test, urine albumin &
creatinine. b) Twenty-four-hour urine tests: The urine may be analyzed for protein
and waste products (urea, nitrogen, and creatinine). c) Glomerular filtration rate:
As kidney disease progresses, GFR fall
25. DIAGNOSIS 2. Blood tests:  Creatinine and urea (BUN) in the blood 
Electrolyte levels and acid-base balance  Blood cell counts  Erythropoietin 3.
Other tests: a) Abdominal ultrasound :Kidneys with CKD are usually smaller (< 9
cm) than normal kidneys. b) Renal Biopsy c) Abdominal CT scan d) Abdominal
MRI e) Renal scan
26. MANAGEMENT Goals of treatment: 1. To preserve renal function 2. To delay
the need for dialysis or transplantation as long as feasible. 3. To alleviate extra
renal manifestations as much as possible. 4. To improve body chemistry values. 5.
To provide an optimal quality of life for the client & significant others.
27. Preserve renal function & delay dialysis: PHARMACOLOGICAL THERAPY:
 Antihypertensive: goal is to keep blood pressure at or below 130/80 mmHg.
ACE inhibitors or angiotensin receptor blockers (ARB) are usually prescribed. 
Cardiovascular agents: diuretics, ianotropic agents.  Antacids: phosphorus
binding antacids  Metabolic acidosis: sodium bicarbonate, dialysis.  Anemia:
Erythropoietin  Control of blood glucose levels.
28. Alleviate extra renal manifestations:  Seizures :Antiseizure agents, safety
measures to protect pt.  Hyper parathyroid: parathyroidectomy
29. Improve body chemistry: Medications  Diet management  Renal
replacement therapy: dialysis , renal transplantation.
30. Dietary management: General dietary guidelines:  Protein restriction:
Decreasing protein intake may slow the progression of chronic kidney disease.
Allowed protein of high biological value.  Salt restriction: Limit to 4-6 grams a
day to avoid fluid retention and help control high blood pressure.  Restrict Fluid
intake
31. Dietary management:  Potassium restriction: High levels of potassium can
cause abnormal heart rhythms. Examples of foods high in potassium include
bananas, oranges, nuts, and potatoes.  Phosphorus restriction: Decreasing
phosphorus intake is recommended to protect bones.  Eggs, beans, cola drinks,
and dairy products are examples of foods high in phosphorus.  High calorie diet
 Vitamin supplements
32. Nursing management Assessment: 1. Complete history taking:  Past &
present history regarding illness, any medication, diet, wt. changes, patterns of
urination etc. 2. Assess pt for the multiple effects of CRF on all body systems. 3.
Assess the pt’s understanding of CRF, the diagnostic tests,& the treatment
regimens. 4. Assess the pt’s need for dialysis. 5. Assess the significant other’s
understanding of the treatment regimen.
33. Nursing diagnosis. 1. Deficient fluid volume or excess fluid volume. 2.
Imbalanced nutrition: less than body requirements. 3. Constipation. 4. Activity
intolerance related to fatigue, anemia, retention of waste products, dialysis. 5. Risk
for impaired skin integrity.
34. Nursing diagnosis. 6. Risk for infection. 7. Risk for injury. 8. Risk for
compromised family and ineffective individual coping. 9. Risk for ineffective
family & individual therapeutic regimen management. 10. Disturbed self- esteem
related to dependency, role, change in body image, & change in sexual function.
35. REFERENCES  Brunner & Suddarth’s, Textbook of Medical Surgical
Nursing.10th ed. Lippincott.  Black M. Joyce, Hawks Hokanson Jane, Medical
Surgical nursing.7th ed.2005, Saunders  http://www.emedicinehealth.com/
Hemodialysis and care of patients.
1. HEMODIALYSIS Mr.Sachin Dwivedi M.SC. Medical surgical Nursing
K.G.M.U Institute of Nursing , Lucknow
2. Mr.Sachin Dwivedi M.SC. Medical surgical Nursing K.G.M.U Institute of
Nursing , Lucknow
3. HEMODIALYSIS It is the removal of solutes and water from body across a
semipermeable membrane (dialyzer)
4. Father of hemodialysis • William Kolf invented the first “artificial kidney”
5. PRINCIPLES underlying HD • Diffusion • Osmosis • Ultra filtration & solvent
drag
6. DIFFUSION • Movement of molecules from an area of higher concentration to
an area of lower concentration
7. OSMOSIS • Movement of solvent molecules from lower concentration to higher
concentration
8. Ultra filtration & Solvent drag • Water moves from an area of high pressure to
an area of lower pressure • More efficient in fluid removal than osmosis •
Molecules which are dissolved in the solvent also get removed- solvent drag
9. INDICATIONS • Acute poisoning • Acute renal failure • Severe edema •
Chronic renal failure • Hepatic coma • Metabolic acidosis • hyperkalemia
10. INDICATIONS…… • Transfusion reaction • Post partum renal insufficiency •
Cardiac tamponade • Fluid overload not responding to diuretics & fluid restriction
11. CONTRAINDICATIONS • Other chronic disease • No vascular access •
Hemorrhage • hypertension • Very old people • Inability to cope with treatment
regimen • Coagulopathy • Inability to survive procedure
12. VASCULAR ACCESS 1. AV FISTULA 2. AV GRAFTS 3. AV SHUNTS 4.
Percutaneous access
13. AV FISTULA • Anastamosis of an artery to a vein • Sites- radial artery &
cephalic vein, brachial artery & cephalic vein, brachial artery & basilic vein • The
increased blood flow and pressure causes the vein to dilate.
14. Pre-op care in AV fistula • Full explanation of the procedure and aftercare • Let
him talk to someone who has a well established fistula • Should be well hydrated
before the surgery • Part preparation
15. Post op care in AV fistula • Limb should be kept warm &well supported to
maintain the peripheral cerculation. • Monitor the BP and maintained at 100
systolic minimum to reduce the risk of fistula thrombosis. • Avoid antihypertensive
therapy • Examine the wound site for bleeding/swelling • Check the blood flow
regularly(bruit/ thrill) regularly
16. Post op care of AV fistula • Avoid using the fistula arm for carrying heavy
loads • Avoid tight and restrictive clothing on the arm. • Hand exercises promote
fistula maturation • Arm should not be used for phlebotomy cannulations or
recording the BP • Notify physician if any bleeding
17. Long term care • Keep your access clean at all times • Be careful not to bump
your access • Don’t wear jewellery over your access • Don’t sleep with your access
arm under your head or body. • Check the pulse in your access every day.
18. Complications of Av fistula • Thrombosis- due to hypotension • Aneurysm-
due to repeated area puncture • Steal syndrome- due to reduced blood
19. ARTERIOVENOUS GRAFT • A graft is put b/w an artery &vein • Synthetic
graft(PTFE) is used most commonly • Indications - Peripheral vascular disease -
Diabetes • Can be used after 14 days
20. AV shunt • Very rarely made • Teflon tubings are inserted into the vessels and
silicon tubings are attached.
21. Percutaneous access • Internal jugular vein • Subclavian vein • Femoral vein •
Indications - Acute dialysis - Temporary - Inadequate vessels - Failed access
22. Percutaneous access
23. Post insertion care • Correct insertion is checked by X-ray • Check for
pneumothorax & puncture of the adjacent vessels • Maintain the patency of the
catheter - Heparin lock injected after each dialysis - Heparin is removed & flushed
with saline (0.9%)before next dialysis - Never flush the catheter if can’t be
aspirated • Examine the sites for any soreness, redness, or presence of exudates
24. Canulation • Allow the fistula to mature • A thorough physical examination is
done before canulating • Adhere to units protocol • Universal precautions are
followed • A tourniquet may be used to get the vessels engorged
25. Types of canulations • Rope ladder puncture • Area puncture • Button hole
puncture
26. Rope ladder technique • The entire vessel is used systematically • Each needle
is inserted at 2cm above the last site and back again • It helps expand the lifespan
of the fistula • Gives the previous stick site time to heal • Helps the fistula mature
more evenly
27. Button hole technique • The same site is repeatedly puncture at exactly the
same angle • Over time the scar tissue develops guiding the needle into the right
place • Advantage - Less pain - Less hematoma
28. Area puncture • Use of one or two areas of the fistula which are regularly used
• Aneurysm chances are more
29. Canulation technique • Needles to be inserted at 45 deg to the skin • Arterial
and venous needle should be placed 5 cm apart • Don’t pull or push the needle
blindly • Ask for assistance if cannulations attempt had failed for 2/3 times
30. HEMODIALYSIS EQUIPMENT • The dialyzer • The membrane
31. Dialyzers • Coiled dialyzers • Parallel plated dialyzers • Hollow fiber dialyzer
32. Membranes • FLUX PROPERTY: the efficiency with which a membrane
clears water and solutes • Cellulose membrane- low flux • Modified cellulose
membrane : low/high flux • Synthetic membrane: low/high
33. Preparation of the dialyzer • Air must be completely removed from the dialyzer
and the bloodlines • Removal of the chemical or the sterilizing agent is essential •
Minimum of 1 lr of saline for flushing in c/o ETO sterilization
34. Dialysate • The fluid which is pumped on the opposite side of the semi
permeable membrane to the patients blood • It is prepared by mixing a
concentrated electrolyte solution with a buffer(bicarbonate) & purified water.
35. Composition of Dialysate SOLUTE BLOOD DIALYSATE SODIUM(mmol/)
130- 149 132-1755 Potassium 3.5- 5 0- 3.0 Urea 2.5 – 6.5 0 Creatinine 60 – 120 0
Calcium(mmol/l) 2.2 – 2.6 0.25 -0. 75 Magnesium 0 – 85 0 – 1.0 Glucose(g/l) 4 –
6.6 0-10 Bicarbonate (mmol/l) 2.2- 3.0 30- 40
36. Anticoagulation • Heparin in the beginning 2000- 5000U or 50 U/Kg and then
as a continuous infusion at 1000- 1500U/hr till 15-60 mts before the end of dialysis
• Heparin free dialysis if bleeding disorder is there.
Nephrotic syndrome
1. Powerpoint Templates Page 1 Peer Group Presentation Subject – Medical
Surgical Nursing Topic - Nephrotic Syndrome Presented by Mr. Hari Singh Nagar
M.Sc Nursing 1st year
2. Powerpoint Templates Page 2 Nephrotic Syndrome Introduction –The syndrome
is apparent in any condition that seriously damage the glomerular capillary
membrane that results in increase glomerular capillary permeability to plasma
proteins. Although liver is capable of increasing the production of protein. It can’t
keep up with the daily loss of albumin through the kidney. Thus hypoalbuminemia
results.
3. Powerpoint Templates Page 3 Definition It is a clinical disorder that is
characterized by proteinuria, hypoalbuminemia, edema and hyperlipidemia. This
occurs due to excessive leakage of plasma proteins in urine because of increase
capillary permeability of the glomerulus.
4. Powerpoint Templates Page 4 Etiology • Glomerulonephritis • DM • SLE •
Amyloidosis o kidney • Sarcoidosis • Cancer • Trauma • Infection • Drugs • Renal
thrombosis
5. Powerpoint Templates Page 5 Pathophysiology
----------------------------------------- Decrease plasma oncotic pressure
Compensatory synthesis of protein including lipoprotein by liver Due to E/F
Glomerular damage Increased permeability of glomerulus capsule to protein
Proteinuria (3.5 gm/24 hours) Increase renal catabolism albumin
Hypoalbuminemia (less then 3.4 mg/DL)
6. Powerpoint Templates Page 6 Hyperlipidemia Fluid escape into the tissue
Decrease plasma volume Edema Decrease GFR Increase Aldosterone Sodium and
water Retention Generalized edema (Anasarca or dropsy) Decrease lipid
catabolism due to low level of protein
7. Powerpoint Templates Page 7 Clinical manifestation • Proteinuria •
Hypoalbuminemia • Edema – Periorbital edema, pitting edema, ankle edema,
Ascites, pleural effusion, Weight gain, hypertension • Fatigue, headache, malaise
and irritability • Foamy appearance of urine (decrease surface tension by severe
proteinuria) • Hematuria • Thrombophilia (clot formation) • Lipiduria • Dyspnoea •
Anaemia
8. Powerpoint Templates Page 8
9. Powerpoint Templates Page 9 Diagnostic evaluation • History • Physical
examination • Urinalysis - 24 hours urine • Serum chemistry • Creatinine clearance
test • Needle biopsy of kidney
10. Powerpoint Templates Page 10 Management 1. Symptomatic treatment •
Edema –  Rest – not for prolong time  Nutrition – 1 gm protein/kg/day, not
more that, sodium restriction, water not greater then the level of diuresis. 
Medication – Loop diuretics (furosemide) • Hypoalbuminemia – moderate intake
of protein, rich in animal protein. • Hyperlipidemia – low saturated fat, high
unsaturated fat, if unresponsive to nutrition therapy then take hypolipidemic drugs
such as statin.
11. Powerpoint Templates Page 11 • Thrombophilia – Heparin • Infection –
Antibiotics • ACE inhibitors – to control hypertension • Achieve better blood
glucose level 2. Kidney damage • Corticosteroid – prednisone •
Immunosuppressant – Cyclophosphamide
12. Powerpoint Templates Page 12 Complication • Infection • Thromboembolic
complication • Pulmonary edema • Hypovolemia • Growth retardation • Altered
drug metabolism • ESRD
13. Powerpoint Templates Page 13 Nursing management 1. Nursing diagnosis –
excessive fluid volume related to damage glomeruli as evidence by I/O chart,
edema and weight gain. Nursing goal – To maintain fluid volume Intervention –
Assess fluid status, Monitor I/O ratio. • Limit fluid and sodium intake to prescribed
volume. • Explain to patient and family rational for fluid resuscitation. • Oral
hygiene is to be encouraged. • To provide the diuretics
14. Powerpoint Templates Page 14 2. Nursing diagnosis – risk of infection related
to edema & altered immune response as evidence by weight gain, I/O chart, taking
temperature. Nursing goal – To prevent from infection Intervention - Limit fluid
intake • Provide meticulous skin care • To monitor I/O chart. • To check daily
weight. • To check the TPR. • Use strict aseptic technique • To provide the
diuretics and antipyretics.
15. Powerpoint Templates Page 15 3. Nursing diagnosis – Disturbed thought
process related to effect of uremic toxin on CNS as evidence by confusion, LOC,
impair ability to process external stimuli. Nursing goal – To stabilise the thought
process Intervention – assess the extent of impairment in thought process. • Orient
to time, place and person. • To provide diuretic, antibiotics to the patient. •
Preserving neurological functioning. • Use seizure precaution.
16. Powerpoint Templates Page 16 • Encourage the patient to turn & in any type of
activity as due to drowsiness and lethargy. • Give psychological support. • Prepare
for haemodialysis.
17. Powerpoint Templates Page 17 Chlorambucil Treatment of Frequently
Relapsing Nephrotic Syndrome Chlorambucil, in combination with prednisone,
was compared with prednisone alone in a randomized controlled trial in 21
children to assess its effect on the duration of remission (improvement) and the rate
of relapse (deterioration after improvement). All control patients treated with
prednisone alone continued to relapse at the same rate, with all patients
experiencing a return of proteinuria by seven months. Conversely, those who
received the same prednisone therapy along with chlorambucil for six to 12 weeks
remained in complete remission, without further medication, during 12 to 34
18. Powerpoint Templates Page 18 months of follow-up observation.
Complications were minimal. Immediate Side effects commonly reported with
cyclophosphamide were not seen with chlorambucil. Comparison with published
reports also suggests that remission induced by chlorambucil is more stable than
that after cyclophosphamide. Chlorambucil appears to be of value in the frequently
relapsing nephrotic patient, adding an effect that is unattainable with prednisone
alone. (N Engl J Med 295:746–749, 1976)
19. Powerpoint Templates Page 19 The effects of corticosteroids on behaviour in
patient with nephrotic syndrome The objective of this study was to measure the
frequency and severity of the behavioural effects of high-dose oral steroid therapy
in children with nephrotic syndrome. We conducted a prospective assessment of
the behaviour of 12 children using a standardized psychological questionnaire at
the time of diagnosis and again after 4 weeks of steroid therapy. A group of control
children was also assessed. There was a significant increase in the total behaviour
score (P=0.03) and specifically in aggressive and poor attention behaviour items in
20. Powerpoint Templates Page 20 the group of nephrotic children compared with
the control group. Four of the children with nephrotic syndrome developed
abnormal behaviour in the clinical range compared with none of the controls. In
conclusion, children with nephrotic syndrome treated with high-dose oral steroids
are at risk of developing clinically relevant behavioural changes
Acute glomerulonephritis
1. ACUTE GLOMERULONEPHRITIS
2. • Abrupt onset of hematuria • Oliguria • Edema • Hypertension
3. ETIOLOGY • 1)post infectious • Strep,staph.hep BnC • 2)Systemic vasculitis •
HSP,Wegener granulamatosis • 3)others • SLE,IgA nephropathy
4. Poststreptococcal GN • AGN following group A hemolytic streptococci •
Infection of throat or skin precedes the onset of nephritis by 1-4 wks
5. PATHOLOGY • Light microscopy-proliferation of mesangial cells and
neutrophil infiltration • Immunofluorescence-granular deposits of IgG n
complement C3 • Electron microscopy-deposits on subepithelial side of GBM
6. Clinical Features • School age children,males Cola coloured urine Puffiness
around the eyes n pedal edema Oliguria HTN Mild proteinuria
7. Lab findings • Urine-1-2+protein with redcells n granular casts • Hemodilution
may result in normocytic anemia • ESR raised • Blood urea n creatinine are
elevated • Hyponatremia n hyperkalemia
8. • ASO titre is increased • Anti DNaseB is elevated • Level of C3 is low
9. MANAGEMENT • Mild oliguria n normal BP –managed at home • 1)diet •
Restriction of Na K n fluids until blood urea reduce n urine output increases •
2)diuretics • Oral furosemide at adose of 1-3mg/kg • Pulmonary edema –IV
frusimide 2-4 mg/kg
10. • 3)Hypertension • Mild –restriction of salt n water intake •
amlodipine,nifedipine or diuretics • 4)LV failure • HTN should be controlled n IV
frusemide given to induce diuresis
11. • 5)prolonged oliguria • Dialysis is indicated in children with severe renal
failure n prolonged oligoanuria,fluid overload n life threatening
electrolytedisturbances
12. CRESCENTIC GN • Rapidly progressive GN(RPGN)-a/c nephritic illness
accompanied by rapid loss of renal function over days to wks • Histopathology-
crescents • Management-initial administration of IV n oral corticosteroids n IV
cyclophosphamide followed by maintenance immunosuppression • Plasmapheresis
in pauci-immune crescentic GN n Goodpasture syndrome
13. NEPHRITIS IN HSP • Most common vasculitis in children • Microscopic
hematuria n mild proteinuria • Serum IgA levels elevate • patient recover without
any treatment • Long term observation is necessary
14. IgA NEPHROPATHY • Deposition of IgA in the glomeruli • Recurrent
episodes of gross hematuria following URI • Patient with hematuria n mild
proteinuria-ACE inhibitors • Nephrotic range proteinuria or deranged renal
function –corticosteroids n alkylating agents
15. LUPUS NEPHRITIS • Variable presentations • Asymptomatic
proteinuria,hematuria ,a/c nephritic syndrome n neephrotic syndrome • Mesangial
n capillary wall deposits of IgG n C3 n usually C1q n IgA • Corticosteroids
,cytotoxic agents,calcineurin inhibitors n monoclonal antibodies n prompt
treatment of infections has improved outcomes