ARF : sudden impairment of renal function ( minute, hours or days ) urea and creatinine serum increas with oliguria ( less than < 400 cc / 24 hr )
Pre Renal : Diminished blood flow : heart failure ; decreased extracellulair / vasculair volume, sodium depletion; dehydration ; shock ; blood loss, water and sodium chloride retention ( earliest ) Filtration and flow tubulus are diminished BUN-Creatinine ratio increase > 20 : 1 ( N = 10 - 20 : 1 )
Intra Renal Acute Tubular necrosis ; Acute Intertitial Nephritis ; Acute Glomerulo nephritis ; severe vasculitis : HUS
Mechanisms : Tubular obstruction > tubular fluid reflux > diminish GBF - - > decrease glomerular function Glomerular demage : Glomerulonephritis acute and vasculitis : infalammatory and immunologic glomerular injury Ishemic : -> Renal blood Supply is blocked > 40 minutes Renal poison : -> metals ; antibiotic ; organic compound ; various metabolic Administration accentuated : dehydration + decrease renal flow
Post Renal : Caused By : Obstruction of the urinary collecting system renal pelvis to urethral orifice Blockage : enlarged prostate; calculi; ureteral compression pelvic / retroperitoneal tumor
Serum creatinine > acurate ( BUN ) for reflects the GFR ( unaffected by exogenous factor as intake protein ) Creatinine clearence the best measurement for functioning nephron Symptoms : weakness; fatigue ; confusion ; tremors ; loss of appetite ; nausea ; vomiting ; bleeding ; malnutrition ; itching ; hypertension ; heart failure
Acidosis : Disturbance acid-basa regulation bicarbonat reabsorbtion distal tubular acid secretion ( renal diseas ) Decreased availability of amonia and urinary phosphat buffers
Fungtion remains intact until the GFR falls to 15 % to 20 % of normal below renal acid becomes inadequade - chronic metabolic acidosis - long priode of time - demineralization of bone. Calcium and phosphorus metabolism
Calcium and phosphorus metabolism GFR falls Creatinine Clearence below 25 cc/min : Serum phosphat increased for the same reasons BUN increased and decreased serum calcium vit. D resistence -> failure of the kidney to convert vit. D 3 from inactive to active stimulation PTH --- > hyperparathyroidism Increased intestinal calcium absorption, bone calcium mobilization and reabsorption renal tubular <<
Skletal demineralization : Increased PTH activity; decreased intestinal absorption of calcium; chronic acidosis; Vit. D resistence
Anemia Normositic normochromic is chareacteristic General depression of erythropoisis bone marrow hypoplasia and decrease reticulocyte Stimulating erythropoitien major cause of anemia of CRF Uremia increase destruction RBC Red cell abnormal hemolytic
Bleeding tendency Uremia --> thrombocyte << ( defective platelet function ) impaire platelet factor 3 and failure platelet aggregation Hypertension Ischemia renal activation of renal angiotension system Sodium over expansion of extracellular fluid volume increase in blood pressure
Laboratory finding Decreased : creatinine clearence Increased : BUN ; creatinine; phosphat; magnesium ( GFR < 30 cc/mnt ); lipoprotein; triglyserides Decreased : calcium ( due to increased serum phosphorus ; decrease cacium absorption and decrease serum albumin ); albumin and total protein ( due to proteinuria )
Increased serum PTH ( response to increased serum phosphorus and decrease serum calcium ) Decreased pH; CO2; ( metabolic acidosis ) ( failure to excrete as acid as NH4 and reabsorp bicarbonat ) Decrease pCO2 ( hyperventilation as compensation metabolic acidosis )
Normocytic normochromic ( hmt 20% - 30% ) Decreased glucose tolerance ( due to impaired cellular utilization ) Decreased urine osmolality Decreased urine spcific gravity ( < 1,020 )
Clearence Creatinine Rumus Cockroft-gault Pria : ( 140 umur ) x BB kg 72 x creatinine serum Wanita : 0,85 x Clearence Creatinine pria Nilai rujukan : 125 100 cc/mnt normal 100 76 cc/mnt insufisiensi ginjal berkurang 75 26 cc/mnt insufiensi ginjal kronik 25 5 cc/ mnt GGK < 5 cc /mnt GGT untuk dilakukan hemodialise