KIDNEY

Biochemical tests for assessing renal

functions
© Dept. of Medical and Clinical Biochemistry UPJŠ in Košice,
Medical Faculty
Eva Ďurovcová, MD. PhD.
5 GM CLB
1
 KIDNEY FUNCTION

1. Control of ECF volume and composition: water, electrolytes, A-B

balance
2. Endocrine - hormone production: renin, calcitriol -1,25(OH)vitD,
erythropoetin
3. Metabolic: 20% of gluconeogenesis
4. Excretion of waste products and toxins: N-compounds (urea,
creatinine, uric acid), drugs, endogeneous metabolites

2
 BIOCHEMICAL TESTS FOR
RENAL FUNCTIONS

1. URINEANALYSIS
2. PROTEINURIA
3. GFR ASSESSMENT
4. TESTS FOR TUBULAR FUNCTION
5
 URINE SAMPLING

 Non-collected sample
 Collected urine

 Storage before analysis

 Analysis up to 1-2 hrs = IDEAL for microscopy
 Refrigerator for about 24hrs
 Chemical preservatives?
 Commercial sampling tubes (up to 72hrs)
 Delay in transportation and analysis results in:
 Bacterial multiplication – metabolize glucose and split urea to CO2 and NH3 (↑pH)
 Evaporation of ketones, oxidation of BIL when exposed to light
 Breakdown of cells in urinary sediment 7
 URINEANALYSIS – PHYSICAL PROPERTIES
1. APPEARANCE:
CLARITY/TURBIDITY: bacteriuria, hematuria, leucocyturia
COLOR: depends on content of urochrome pigments concentration of urine
Light yellow to colourless: after larger fluid intake, diabetes mellitus, insipidus

2. ABNORMAL COLOR:
DARK YELLOW - ORANGE: dehydration, bilirubin, carrotens,
PINK-RED-BROWN: Hb, myoglobin, RBC, porphyrines, rifampicin, food- beetroot, senna,
rhubarb...
BROWN-BLACK: bilirubin, urological tea, melanine (melanoma), homogentisic acid
(alcaptonuria)
BLUE-GREEN: methylene blue, riboflavin, propofol, infections (Pseudomonas)
8
URINARY SEDIMENT
examination of the sediment obtained
by centrifugation of a fresh urine
sample (up to 1 hour)
- organic and anorganic elements

NORMAL FINDING:
few cells (RBC, leukocytes, epithelia
from lower UT)
hyaline casts rarely
PATHOLOGICAL:
 increased number of all components
 other types of casts and crystals

11
HEMATURIA – RBC (PHASE CONTRAST MICROSCOPY)

acanthocytes Renal (glomerular) hematuria:

dysmorphic RBC (deformation during
crossing of GBM) - acanthocytes
CAUSE: Glomerulonephritis (mainly
autoimmune with immunocomplexes
deposition)

Nonglomerular (postrenal)
hematuria: isomorphic RBC (non-
deformated)
CAUSE: bleeding from renal or UT
parenchyme
bleeding - stones, inflammation,
tumours,injury

12
LEUKOCYTURIA – PMN

Massive leukocyturia: -
leukocytes with damaged
membrane have typical
dark-coloured nuclei,
- less damaged cells are
still non-coloured

13
CYLINDERS
- are formed only in the distal convoluted tubule or
the collecting duct (distal nephron) – mostly during
oliguric, anuric phase of disease:
- high concentration of urine,
- slow rate of urine flow,
- high protein concentration

Composition: Tamm-Horsfall mucoprotein

=orosomucoid
 Protein cylinders
 Cellular cylinders

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 CRYSTALS

Crystalisation depends on urinary pH :

1. Acidic urine: uric acid (various shapes), calcium oxalate
2. Alkaline urine: phosphates
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 URINARY SEDIMENT - ABNORMALITIES

 Formed elements (RBC, leukocytes, cellular casts) in sediment may indicate acute
or chronic glomerular, tubulointerstitial, or vascular kidney disease
 Dif. DG of pathological finding requires correlation of urine analysis with other
clinical markers

Examples:
HEMATURIA: any type of renal or urological diseases
LEUKOCYTURIA + CYLINDERS: inflammatory renal disease (pyelonephritis)
LEUKOCYTURIA without CYLINDERS: lower urinary tract infection (UTI)
+ bacteriuria
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 PROTEINURIA

 early diagnosis of kidney disease

 monitoring their progression
 assessing therapeutic response
 estimation the risk of renal failure

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 PHYSIOLOGICAL PROTEINURIA
Glomerular ultrafiltrate contains ~ 30 mg/L proteins
Does not exceed 150 mg/D (=arbitrary value) v.afferens v.efferens

Origin of proteins in urine:

 60 – 80% renal:
 orosomucoid = Tamm-Horsfall´s mucoprotein

 20 – 40% plasma:

t
 albumin

tubulus
 LMW proteins – FLC of Ig, tissue degradation
products

 Urinary tract:
 IgG a IgA
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PATHOLOGICAL PROTEINURIA

proteinuria

prerenal renal postrenal

glomerular tubular

selective nonselective
Details on seminars...
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 SCREENING FOR PROTEINURIA
1. Urine strips
 react mostly with albumin
 limit of detection: 100 - 150 mg/L (concentrated
morning urine)
 false negativity: LMW proteins + globulins
 false positivity: concentrated urine, hematuria,
alkaline pH

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 ...TESTING OF PROTEINURIA
If positive screening with urine strips, then:

2. step: Protein/creatinine ratio (PCR) in random urine sample (1st or 2nd morning
sample )
PCR <15 mg/mmol creat (e.g. 150 mg protein/10 mmol creatinine)

3. step: Quantitative proteinuria - in collected urine: <150 mg/D

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 ALBUMINURIA

 marker of incipient chronic renal disorders (GNF)

 risk groups of patients: DM and hypertension
 Marker of endothelial dysfunction
 Positive test in patient with negative finding of U-protein - more sensitive
immuassay (100-times higher sensitivity)

SCREENING FOR ALBUMINURIA

 Spot urine sample (1st or 2nd morning sample)
 2 from 3 urine samples during 6 months should be positive for confirmation
(40% day-to-day variability)
 Interfering factors: lack of fluids/concentrated urine, stress, physical activity, UTI
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 ALBUMINURIA

microalbuminuria

Increased Severe
Parameter Normal
albuminuria albuminuria
ALB mg/l < 20 20 - 200 > 200

ALB µg/min < 20 20 - 200 > 200

ALB mg/ mmol creat <3 < 30 > 30

F 29
 HEMATURIA - CAUSES
Type Causes Condition or disease
Renal - Glomerulonephritis IgA nephropathy, SLE, Goodpasture
glomerular Systemic diseases syndrome, thin basement membrane
Hereditary nephropathies disease,
Alport´s syndrome

Renal - Tubulointerstitial disorders Nephritis, acute tubular necrosis,

nonglomerular Tumours, trauma, stones, febrile Hydronephosis,
illnesses Grawitz, Wilms tumour

Postglomerular UTI, bleeding, nephrolithiasis, Cystitis, urethritis, prostatitis,

Prostate diseases BPH, prostate biopsy,
Urogenital mucosal injuries, Metabolic Radiotherapy, cathetrization,
causes Hypercalciuria, hyperuricosuria
Tendency to bleeding Thrombocytopenia, coagulopathy
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 MEASUREMENT OF
GLOMERULAR FILTRATION RATE

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 GLOMERULAR FILTRATION RATE (GFR)

Most frequently indicator of kidney function:

 for diagnostics and monitoring
 to adjust the dose of some drugs excreted by the kidneys
 to evaluate the development of renal insufficiency, or indicate an
extracorporeal eliminating method

1. Estimated GFR based on S-creatinine concentration

2. Creatinine clearance
3. Calculation from cystatin C
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 CREATININE
 Endogenous product of muscle metabolism (derived from creatine-P)
 Production is fairly constant from day to day - determined by muscle mass
(rather than its activity)
 Method and sex-dependent reference intervals:
 S-creatinine: 45 – 90 μmol/L (women)
55 – 110 μmol/L (men)
Urinary excretion of creatinine: 2 – 20 mmol/24 hrs

 Elimination: GF + TS (<10% is secreted into urine )

(SMALL OVERESTIMATION of GFR !!!)
 Serum creatinine as an index of GFR
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 RELATIONSHIP BETWEEN GFR AND S-CREA
Stages of CKD
5 4 3 2 1
1 000

S-Creatinine (μmol/L)
800

A ↔ B illustrate the large

D change in GFR that results
C ↔ D illustrate the 500 from a small change in
small change in GFR creatinine clearance
serum creatinine at higher
that results from a C levels of kidney function
large change in serum real GFR
creatinine at lower 100
B A
levels of kidney
function 0.25 0.5 1 1.5 2
GFR(mL/s)
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 I. ESTIMATED GFR (eGFR)

MDRD (Modification of Diet in Renal Disease)

 derived from large multicentric study concerned the influence of low protein intake on
progression of CKD (18-70 y)
 Underestimate GFR for individuals with serum creatinine at the upper limit of normal
(MEN, ELDERLY).

CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration, 2012)

 Based on 10 studies (>8000 participants with/without CKD)
 More accurate than MDRD
 compared with the MDRD equation, 24.4% of patients were re-classified to a higher
GFR category (CKD)
Levey AS et al, JAMA 2012;307(18): 1941-1951
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 PURPOSE OF USE eGFR
 screening of CKD
 rapid estimation of GFR in non-acute patients
 NOT valid in the setting of pregnancy or extremes of body mass or in
children under 18 y of age

In children: SCHWARTZ´s formula

eGF= F x S-Cr x hight (cm), F=factor depending on age

COCKROFT´s formula - no longer recommended

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 LABORATORY REPORT

eGFR > 1.5 ml/s (90 ml/min) = kidney dissease excluded

eGFR 1.5 – 1.0 ml/s = grey zone
eGFR < 1.0 ml/s (60 ml/min) = (chronic) kidney disease

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 II. CREATININE CLEARANCE
 Clearance is volume of plasma „cleared“ of the particular substance per minute/second
 If a substance is freely filtered by glomeruli and is not secreted into or reabsorbed from
the urine, then the clearance = GFR

 No substance is cleared completely from plasma this way !

 CREATININE
 GFR estimation requires measurement of serum/plasma concentration S(P) and
urinary excretion rate U*V

In health Ccr = GFR, BUT Ccr overestimates real GFR in advanced CKD
 In normal kidney: GF (only <10% TS)
 Renal failure: GF + secretion in tubules (up to 50%)
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 CREATININE CLEARANCE – CALCULATION

2 samples: 4 variables:
 Sample of blood: S-Cr
 24 h collected urine: U-Cr
volume (mL)
time (min,s)
Weight, hight: correction for ideal BSA
C cr = U-Cr x V
S-Cr
 GFR corr = Ccr x 1.73/m2
 RH 1.5 – 2.5 mL/s
 Age and sex dependent values !!!
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 CREATININE CLEARANCE – LIMITATIONS

1. Laboratory methods for CREATININE:

 Jaffe - non-specific – measure non-creatine chromogens
 Enzymatic method – more specific
2. Concentration of S-Cr depends on:
 muscle mass,
 diet (stewed meat),
 other substances* that interfere with method (ketones, GLU, BIL, cephalosporins...)

 Tubular secretion: increases in RF, some medicine ↓tubular secretion

 Inacuracy in urine sampling and volume measurement

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 III. GFR ESTIMATED FROM CYSTATIN C

Cystatin C – small polypeptide (13 kDa), inhibitor of cysteine proteases

 Produced by all nucleated cells - very stabile concentration in blood
 Freely filtratedin glomeruli and is fully metabolized by tubular cells
 If GFR decreases - ↑ cystatin C in serum/plasma when

 More sensitive and earlier marker of decrease in GFR than C-Cr

 Grubb´s formula for estimated GFR:

eGFR = 1.4115 x S-cystatin C-1,680 x F;
F=differs in M,F and CH
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 III. eGFR FROM CYSTATIN C

Can be used in patients:

 who have lost muscle mass (longterm
immobilisation, muscle dystrophy, malnutrition,
amputation of extremities)
 who have decreased GFR estimated from S-
creat, mainly if other markers of renal damage
are missing
 whom S-creat concentration is affected
(pregnancy, edemas, small children,....)
 who need careful monitoring of renal functions
– after Tx
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 eGFR FROM CYSTATIN C

Limitations of use:
 ↑ GC excess, corticotherapy
 ↑↓ thyroid disorders
 ↑ rapidly proliferating tumours

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 UREA

 S-UREA is used as an additional marker of renal function

 synthesized in the liver as an endproduct of protein catabolism (deamination of
AA - ammonia)
 Serum: 2.5 – 8.5 mmol/L
 elimination in the urine = major route for nitrogen excretion → 300- 600
mmol/D

CONDSIDER RENAL and EXTRARENAL INFLUENCES !!!

 ↑ urea (increase without or more than CREAT): high protein intake, catabolic states
(burns, sepsis, absorption of AA after GI hemorrhage) dehydration,
 ↓ urea: protein malnutrition, severe liver diseases (low synthesis!), hyperhydration
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 ASSESSMENT OF TUBULAR
FUNCTIONS

 Resorption  AA, GLU, P...

 Secretion  H+
 Dilution-concentration  water - polyuria
 A-B regulation  acidosis

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 FRACTIONAL EXCRETION
Amount of filtered substance (GF) = excreted (fraction excretion, FE) + reabsorbed
(tubular resorption, TR) amount
 GF = FE + TR = 100%
Example: 180 L of glomerular ultrafiltrate = 1.8 L (diuresis=1%)
+ tubular resorption (99%) → FE-H2O = 1%

FRACTIONAL EXCRETION = FE = Csubst/Ccreat

Sample: random urine + blood (serum)

Lab: measures concentration of substance + creatinine in serum + in urine and calculate FE
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 CHANGES OF FE IN FAILING KIDNEY
 Despite FE is a marker of tubule functions, it is not quite independent of the GFR.
 If GFR decreases with unchanged FE water → diuresis decreases → retention of water and
waste products.
 Adaptation of residual nephrons :
→ increase of FE water+solutes
→ prevents their retention

The mechanism allows maintenance of diuresis and excretion of LMW substances per
surviving nephrons
 Glomerulo-tubular balance → tubular functions compensate for changes in GFR
53
 CLINICAL SIGNIFICANCE OF FE

 Frequently used FE of water and LMW (Na, K, Ca, Cl, Mg, P, H20)

 helps to assess, wheather kidney works normally or some adaptation

processes have occured due to renal disease

 to assess of retention or depletion of electrolytes in the body

 to distingiush between osmotic and water diuresis

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 NORMAL VALUES OF FE

Parameter Normal value Change in FE

• tubular compensation of ↓GFR

0.010 – 0.020 • disorders of tubular reabsorption
FE Na 1 – 2% • diuretics
• osmotic diuresis (glukose, calcium, mannitol...)
• tubular compensation of ↓GFR
0.040 – 0.190 • diuretics
FE K 4 – 19% • hypercatabolism
• hyperaldosteronism

FE H2O 0.004 – 0.012

Isostenuria: FE H2O = FE osm
0.4 – 1.2%
 If patient does not reach these maximal values, we could try
FE osm <0.035
increase FE Increased in osmotic diuresis
diuretics to<3.5%
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 NORMAL AND MAXIMAL VALUES OF FE
Parameter Normal value Maximal value Example

FE Na 0.010 – 0.020 0.350 patient on loop diuretics: 0.033 *

FE K 0.040 – 0.190 1.5 – 2.0 patient with hypokalemia: 0.020**

FE H2O 0.004 – 0.012 0.3 – 0.4 ***FE H2O = FE osm

FE osm <0.035 0.035 Increased in osmotic diuresis

* Could we try to increase dosing of diuretics in order to increase renal excretion of Na ?

** What does low FE-K mean ?
*** What does it mean?
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 CONCENTRATION - DILUTION

 Obligatory solute load excreted by kidney is 600 mmol/D → urine volume of 2 L/D
will be required (if U-osmolality = 300 mmol/kg water)
 Normal kidney can achieve extreme osmolalities 50 – 1200 mmol/kg depending on
hydration
 Person with normal renal function is able to excrete daily solute load in 500mL/D or
15L/D
 Diseased kidney (=loss of concentrating ability) is able to achieve osmolalities close
to 300 mmol/kg (= isostenuria)

62
 ↓ CONCENTRATING ABILITY
 Decreased osmotic gradient in renal medulla (countercurrent mechanism -
loop of Henle, vasa recta):
 Anatomical deformation of medulla
 Decreased tubular transport
 Disorders of intrarenal blood flow
 Lack of ADH

Lab tests:
1. U-osmolality
2. FE-water, FE-osm
3. Adiuretine test

63
 FAILURE OF CONCENTRATING ABILITY

Causal mechanism Examples

Lesions of supraoptic-hypothalamic-hypophyseal (CNS)
Lack of ADH/vasopressin secretion
system (trauma, tumours...)
lesions of the thirst centre causing polydipsia,
Inhibition of ADH release
psychogenic polydipsia,
Inability of tubules to respond to Nephrogenic diabetes insipidus (renal tubular defects,
ADH Fanconi syndrome)
Chronic renal failure, hydronephrosis,, renal papillary
Inability to maintain renal
necrosis (analgetics)
medullary hyperosmolality
hypokalaemia, hypercalcaemia

Increased solute load per nephron Osmotic diuresis: Diabetes mellitus

64
 CONCENTRATING TEST
1. Fluid deprivation: up to 24 hours
2. Adiuretine/desmopressin test: ADH analoge (DDAVP)
 Serum osmolality (275 – 295 mmol/kg) should not increase
 Urine osmolality: At least one portion of urine should reach target osmolality
depending on age (800 mmol/kg or more):

age U-osmolality(mmol/kg) U-osm/S-osm

15 – 20 970 3.34
21 – 50 940 3.21
51 – 60 830 2.86
61 – 70 790 2.72
71 – 80 780 2.69 65
 ACIDIFICATION AND ALKALINIZATION OF URINE
 Indication for testing = Renal tubular acidosis (RTA)
 Metabolic hyperchloremic acidosis (NO diarrhea!!) – due to failure of kidney to
excrete H+ excess (DISTAL TUBULE) or to absorb HCO3- (PROXIMAL TUBULE)
 Despite systemic acidosis kidneys are not able to produce acidic urine
 Tubulopathy may be inherited or aquired, isolated defect or combined (Fanconi
syndrome

 DIAGNOSTIC tests:
 Urinary pH after acidifying substance load = ACIDIFICATION test
 FE-HCO3- = ALKALINIZATION test

66
 Renal failure - definition

Rapid and sustained decrease in renal function with:

 Retention of N-compounds, H+, other metabolic products
 Oliguria < 400 ml/D (usually, but not always)

Terminology:
 Chronic Renal Failure ≈ pathophysiology
Chronic Kidney Disease (CKD) Stage (1, 2,) 3a, 3b, 4, 5 (IDC)

 Acute Renal Failure (ARF) ≈ pathophysiology

Acute Kidney Injury (AKI) Grade 1, 2 or 3 (IDC)

70
 AKI simplified
Stage 1
 Creatinine increased by 27 umol/L > 120
 or urine output < 40 ml/hr x 6 hrs
Stage 2
 Creatinine increased x 2 2x normal
 or urine output < 40 ml/hr x 12 hrs or > 240
Stage 3
 Creatinine increased x 3 or >354 umol/L or dialysis 3x normal
 or urine output <25 ml/hr x 24 hrs or > 360
Kellum JA, Levin N, Bouman C, et al. Developing a consensus classification system for acute renal failure. Curr Opin Crit Care (2002) 8:509–514

The biochemical clues =

+ rapidly rising S-creatinine (urea, UA) concentration
+ hyperkalemia
+ metabolic acidosis. 71
 AKI PRERENAL - 30 – 60%

CAUSES: volume depletion from any etiology with renal hypoperfusion. The decrease in
renal plasma flow (RPF), will decrease GFR.
1. Dehydration
2. Hemorrhage
3. Severe diarrhoea, vomiting
4. Post-operative fluid and blood losses
5. Sepsis
6. Acute heart failure

Compensation – what happens when renal plasma flow (RPF) falls ?

a. vasodilatation of the afferent arteriole - local prostaglandin production
b. vasoconstriction via angiotensin II
c. redistribution of renal blood flow → more for tubules
d. stimulation of R-A-A system and ADH secretion → small volume highly concentrated urine
with ↓Na (FE-Na < 1%) 73
 AKI RENAL - 20 – 40%

CAUSES EXAMPLES
Specific renal diseases and systemic Rapidly progressive GNF, SLE
diseases affecting glomeruli
Ischaemia (stop in blood supply) → Bleeding, sepsis, sepsis, hypovolaemia,
tubular necrosis
Nephrotoxins Aminoglycosides, cephalosporins, cisplatinum,
- direct nephrotoxicity NSAID
- drug induced allergic reaction Contrast nephropathy - Iodinated contrast agents

Vascular Small and large vesels

Intrarenal obstruction Myeloma – cast nephropathy
Tumour lysis syndrome
74
 AKI POSTRENAL - 5 – 15%
„When the plumbing is clogged the kidneys fail“.

Bilateral (rarely unilateral) obstruction of the urine flow ↑hydrostatic pressure

which acts in opposition to GF →tubular necrosis
 Intrarenal: crystals, proteins (monoclonal, cryoglobulins)

 Extrarenal : (Pelvis/Ureter/Bladder/Urethra/Prostate)

 Men: prostatic hypertrophy, cancer

 Women: cervical cancer

DIAGNOSIS: Labs are not usefull !!!

 Ultrasound
 Foley´s cathether (after void residuum >200 mL)
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 AKI – DIF. DIAGNOSIS

PARAMETER PRERENAL RENAL

U-Cr/S-Cr ratio > 40 < 10
U-Na <20 mmol/L > 40 mmol/L
FE-Na < 1% > 1%
U-osmolality > 500 mmol/kg < 300 mmol/kg
U/S-osmolality > 1.5 ≤ 1.0
U-sediment Normal or hyaline casts Casts, tubular epithelial
cells

Many limitations, lack of specificity

77
 AKI – DIF. DIAGNOSIS

S-urea 13 mmol/L PARAMETER PRERENAL RENAL

S-Creat 182 µmol/L U-Cr/S-Cr ratio > 40 < 10
U-Na 61 mmol/L U-Na <20 mmol/L > 40 mmol/L
U-Cr 4.99 mmol/L FE-Na < 1% > 1%
U-osm 320 mOsm/kg
U-osmolality > 500 mmol/kg < 300 mmol/kg

FE-Na 3.4% (0.034) U/S-osmolality > 1.5 ≤ 1.0

U-sediment Normal or hyaline Casts, tubular
casts epithelial cells
Prerenal or renal ?
79
 CHRONIC KIDNEY DISEASE
Progressive irreversible impairment of renal function with decrease in the number of
functioning nephrons
stage GF (ml/s/1,73 m2) other

+ proteinuria or abnormal USG (early diabeteic

CKD 1 ≥ 1.5
nephropathy - hyperfiltration)
CKD 2 1.0 – 1.49 + proteinuria or abnormal USG
Most prevalent (do not need other markers of kidney
CKD 3 0.5 – 0.99
damage)
One in five of these patients
CKD 4 0.25 – 0.49
will be on dialysis in the next five years.
These patients are on
CKD 5 < 0.25
dialysis or dialysis is imminent.
CKD 5D Dialysis, Tx 81
 DIAGNOSTIC CRITERIA FOR CKD
Decrease GFR Markers of kidney injury

<60 ml/min/1.73 m2  albuminuria (ACR ≥3 mg/mmol, dU-Alb ≥30 mg/24 hours),

 pathological urinary sediment
 ion and other abnormalities due to tubular disorders,
 pathological histological finding (biopsy),
 structural abnormalities in imaging studies
<1 ml/s/1.73 m2
 history of kidney transplantation

83
 SCREENING FOR CKD – population at risk:
 Diabetes mellitus Screen according national
 Hypertension recommendations every 1-2 years
depending on clinical circumstances
 CVD using serum creatinine (eGFR) and
 Acute renal disorders random urine tests (ALB/creat

ratio=ACR).
Systemic disorders with possible renal imairment
 Positive family history of kidney disease
In the absence of kidney damage, an eGFR >60 mL/min is not
kidney disease!
Modest fluctuation in creatinine/eGFR are common - do not
diagnose CKD based on one single test!
CKD diagnosis requires persistence of abnormalities
84
 METABOLIC CHANGES IN CKD
Metabolic feature INCREASED DECREASED
1. Nephrotic syndrome: A. Patients are edematous but typically
2. Nephritic syndrome: An inflammatory glomerular injury.
Impaired
 urinaryproteinuria(though
hematuria, concentration not as much as Osmolality in settings
 with nephrotic syndrome) RBC casts (variable). of hypervolaemia
and dilution
 renal failure and hypertension. This is an important
 cause of ARF
Disturbance of electrolyte and K+ Na+
hydrogen ion homeostasis H+ (MAC) HCO3

Retention of waste products of Creatinine, urea,

metabolism uric acid

Impaired calcitriol synthesis P, Mg, PTH Calcitriol→ Ca

Low erythropoetin synthesis RBC (anaemia)

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 NAME OF PRESENTATION
Company name

Any questions ???