This document discusses acute kidney injury and chronic kidney disease. It covers the pathophysiology, management, investigations and treatment of AKI, stages and causes of CKD, signs and symptoms of CKD, and supportive treatments for CKD including diet, controlling blood pressure and diabetes, treating anemia and bone disease, and use of diuretics and dialysis.
This document discusses acute kidney injury and chronic kidney disease. It covers the pathophysiology, management, investigations and treatment of AKI, stages and causes of CKD, signs and symptoms of CKD, and supportive treatments for CKD including diet, controlling blood pressure and diabetes, treating anemia and bone disease, and use of diuretics and dialysis.
This document discusses acute kidney injury and chronic kidney disease. It covers the pathophysiology, management, investigations and treatment of AKI, stages and causes of CKD, signs and symptoms of CKD, and supportive treatments for CKD including diet, controlling blood pressure and diabetes, treating anemia and bone disease, and use of diuretics and dialysis.
This document discusses acute kidney injury and chronic kidney disease. It covers the pathophysiology, management, investigations and treatment of AKI, stages and causes of CKD, signs and symptoms of CKD, and supportive treatments for CKD including diet, controlling blood pressure and diabetes, treating anemia and bone disease, and use of diuretics and dialysis.
• Rapid ,<48hours deterioration/impairment of kidney function resulting in the retention of nitrogenous and other waste products normally cleared by the kidneys • creatinine clearance going down >50% and or creatinine increasing more than 0.3mg/dl or urine output less than 0.5ml/g/hr for 6 hours pathophysiology • With renal hypoperfusion from decreased cardiac output or low blood pressure vasoconstriction of efferent arteries occurs. • This is mediated by renin-angiotension-aldosterone axis,vasopressin and sympathetic system.this way glomerular filtration can be maintained even with hypoperfusion. • Afferent vasodilation also occurs via nitric oxide and prostaglandins maintaining glomerular perfusion • This autoregualtion fails if prolonged and when BP fall to less than 80mmhg systolic hence AKI management • Treat underling cause eg sepsis,heart failure,GE • Avoid nephrotoxic insults e.g drugs • Optimize bp,keep MAP(>60mmhg) • Watch for electrolytes and fluid balance • Relieve obstruction if present • Indication for acute dialysis • Acid base abnormalities-metabolic acidosis • Electrolyte e.g hyperkalemea,hypercalcemea, • Fluid overload-pulmonary edema • Uremea-pericarditis,encephalopathy,bleeding Investigations-AKI/CKD • Serial Urinalysis,urine output,osmolarity • Fractional excretion of sodium e.g <1% in pre- renal vs >2% in acute tubular necrosis • Urea,electrolte and creatinine • Calcium,phosphatevitamin D,parathyroid levels hemoglobin normal in AKI abnormal in CKD • Serologies-looking for glomerular disease eg HIV,ANA,HEPB/C,P-ANCA.C-ANCA etc • Renal ultrasound-size of kidneys,normal in Aki,small in CKD CKD • >3 months of reduced glomerular function of <60ml/min and or renal damage (imaging,pathology,markers) Stages of CKD aetiology • Diabetic glomerular disease • Glomerulonephritis eg post streptococcal,connective tissue disease, • Hypertensive nephropathy Primary glomerulopathy with hypertension Vascular and ischemic renal disease • Autosomal dominant polycystic kidney disease • Other cystic and tubulointerstitial nephropathy • Urological causes-BPHH,bladder tumor Signs and smptoms • Majority are asymptomatic till late • Uremic syndrome from urea other waste products accumulation cause symptoms late on • General-nausea,anorexia,malaise,fetor • Skin-uremic frost,pruritus • Neurologic-encephalopathy(decreased mental status,memory,attention)seizures,neuropathy • Cardiovascular-pericarditis, LVH,hypertension,cardiomyopathy,CAD,heart failure • Haematology-anemia,bleeding,thrombocytopnea • Metabolic-hyperkalemea,acidosis • Bone mineral disease- hypocalcemea,hyperphosphotemea results in hyperparathyroidism :osteoarthropathy with osteitis fibrosa cystica,adynamic bone disease,osteomalacia • Endocrine-sexual dysfunction,low VITD,impaired growth and development,infertility • Other manifestation-fluid retention,acid-base abnormalities ,dyslipidemea • Systemic inflammation-low albumin,cachexia,accelerated atherosclerosis • Anemea is universal at stage 4 and 5 CKD – Reduced erythropeitin production by kidneys – Increased bleeding due to uremea – Reduced levels of haematinics-fe,B2,folate – Iron deficiency – Reduced RBC survival span – Comorbidities-autoimmune,HIV,drugs etc – Hyperparathyroidism and bone marrow fibrosis – Chronic inflammation treatment • Supportive- – Diet-low salt diet,low phosphate,low potassium – Control DM HBA1C <7% – HTN-BP 130/80 ACE-I/ARB if not hyperkelemic and creatinine <250mmol/l – Anemia-target HGB 11-12g/dl erythropoetin injection with injection iron – Secondary hyperparathyroidism -from low calcitriol,calcium and high phosphate causing osteodystrophy – If calcium low and phosphate high use calcium carbonate(actal tums) or phosphate binders eg sevelamer – Vitamin D (calcitriol) • Diuresis – Loop diuretics eg furosemide 40mg bd-tid,torsemide 20mg.a/e-hypokalemea,hyponatremea,hypocalcemea – Thiazide –HCTZ 25mg metolazone 2.5mg.as above but hypercalcemea,hyperlipidemea,hyperuricemea – Mineralocorticoid inhibitor- spirinolactone.hyperkalemea,gnacomastia • Dialysis-water,toxins and electrolytes control – Perioteneal dialysis and haemodialysis • Renal transplant