The Pathophysiology Of Acute Renal Failure

1. PATHOPHYSIOLOGY OF ACUTE RENAL FAILURE Bayu F. Wibowo Bag. Ilmu Bedah FK UNAND

2. Introduction The sudden interruption of renal function 5% of all hospitalized patients  acute renal failure. Prerenal , intrarenal , or postrenal Three distinct phases: oliguric , diuretic, and recovery. Treatment (+)  Reversible Treatment (-)  E nd-stage renal disease, prerenal azotemia , and death.

3. ACUTE RENAL FAILURE The glomerular filtration rate is reduced, Sudden retention of endogenous and exogenous metabolites ( urea, potassium, phosphate , sulfate, creatinine , administered drugs), The urine volume is usually low (under 400 mL /day ).

4. Causes Arrhythmias Cardiac Tamponade Cardiogenic Shock Heart Failure Myocardial Infarction Burns Dehydration Diuretic Overuse Hemorrhage Hypovolemic Shock Trauma Antihypertensive Drugs Sepsis Arterial Embolism Arterial Or Venous Thrombosis Tumor Disseminated Intravascular Coagulation Eclampsia Malignant Hypertension Vasculitis . Prerenal Failure

5. Poorly Treated Prerenal Failure Nephrotoxins Obstetric Complications Crush Injuries Myopathy Transfusion Reaction Acute Glomerulonephritis Acute Interstitial Nephritis Acute Pyelonephritis Bilateral Renal Vein Thrombosis Malignant Nephrosclerosis Papillary Necrosis Polyarteritis Nodosa Renal Myeloma Sickle Cell Disease Systemic Lupus Erythematosus Vasculitis . Intrarenal Failure

6. Bladder Obstruction Ureteral Obstruction Urethral Obstruction Postrenal Failure

7. Pathophysiology Prerenal failure  blood flow to the kidneys leads to hypoperfusion . Azotemia  consequence of renal hypoperfusion  excess nitrogenous waste products in the blood  develops in 40% to 80% of all cases of acute renal failure. Renal blood flow is interrupted  oxygen delivery  hypoxemia and ischemia  damage the kidney. Glomerular filtration rate (GFR)  electrolyte imbalance and metabolic acidosis Tubular reabsorption of sodium and water Prerenal Failure

8. Intrinsic or parenchymal renal failure  damage to the filtering structures of the kidneys Causes of intrarenal failure are classified as nephrotoxic , inflammatory, or ischemic. Nephrotoxicity or inflammation  the delicate layer under the epithelium irreparably damaged. Severe or prolonged lack of blood flow by ischemia  renal damage (ischemic parenchymal injury) + excess nitrogen in the blood (intrinsic renal azotemia ). The fluid loss  hypotension  ischemia  ischemic tissue  toxic oxygen-free radicals  cause swelling, injury, necrosis. The necrosis caused by nephrotoxins tends to be uniform and limited to the proximal tubules, whereas ischemia necrosis tends to be patchy and distributed along various parts of the nephron . Intrarenal Failure

9. Bilateral obstruction of urine outflow (the bladder, ureters , or urethra)  postrenal failure Bladder obstruction  anticholinergic drugs, autonomic nerve dysfunction, Infection, tumors. Ureteral obstructions  blood clots, Calculi, edema or inflammation, necrotic renal papillae, retroperitoneal fibrosis or hemorrhage, surgery, tumor or uric acid crystals. Urethral obstruction  prostatic hyperplasia, tumor, or strictures. Postrenal Failure

10. Three Distinct Phases Oliguric phase Necrosis of the tubules  cause sloughing of cells, cast formations, and ischemic edema  resulting tubular obstruction  a retrograde increase in pressure and a decrease in GFR  increase tubular permeability and cause backleak . Intrarenal release of angiotensin II or redistribution of blood flow from the cortex to the medulla  constrict the afferent arterioles  increasing glomerular permeability and decreasing GFR. Urine output  less than 30 mL /hour or 400 mL /day for a few days to weeks. The kidneys respond to decreased blood flow by conserving sodium and water.

11. Diuretic phase Marked by increased urine secretion of more than 400 ml/24 hours, ensues. GFR may be normal or increased, but tubular support mechanisms are abnormal. Excretion of dilute urine causes dehydration and electrolyte imbalances. High blood urea nitrogen (BUN) levels produce osmotic diuresis and consequent deficits of potassium, sodium, and water. The diuretic phase may last days or weeks.

12. Recovery phase Azotemia gradually disappears and recovery occurs. The recovery phase is a gradual return to normal or near-normal renal function over 3 to 12 months.

13. Signs And Symptoms Oliguria due to decreased GFR Tachycardia due to hypotension Hypotension due to hypovolemia Dry mucous membranes due to stimulation of the sympathetic nervous system Flat neck veins due to hypovolemia Lethargy due to altered cerebral perfusion Cool, clammy skin due to decreased cardiac output and heart failure Progressive symptoms : Edema related to fluid retention Confusion due to altered cerebral perfusion and azotemia GI symptoms due to altered metabolic status Crackles on auscultation due to fluid in the lungs Infection due to altered immune response Seizures and coma related to alteration in consciousness Hematuria , petechiae , and ecchymosis related to bleeding abnormalities

14. Complications Chronic Renal Failure Ischemic Parenchymal Injury Intrinsic Renal Azotemia Electrolyte Imbalance Metabolic Acidosis Pulmonary Edema Hypertensive Crisis Infection

15. Diagnosis Blood studies  elevated BUN, serum creatinine , and potassium levels; decreased bicarbonate level, hematocrit , and hemoglobin; and acid ph Urine studies  casts, cellular debris, and decreased specific gravity; in glomerular diseases, proteinuria and urine osmolality close to serum osmolality ; sodium level less than 20 meq /L if oliguria results from decreased perfusion, and more than 40 meq /L if cause is intrarenal Creatinine clearance test measuring GFR and reflecting the number of remaining functioning nephrons Electrocardiogram (ECG) showing tall, peaked T waves; widening QRS complex; and disappearing P waves if hyperkalemia is present Ultrasonography , plain films of the abdomen, kidney- ureter -bladder radiography, excretory urography , renal scan, retrograde pyelography , computed tomographic scans, and nephrotomography

16. Treatment High-calorie diet that's low in protein, sodium, and potassium to meet metabolic needs I.V. Therapy to maintain and correct fluid and electrolyte balance Fluid restriction to minimize edema Diuretic therapy to treat oliguric phase Sodium polystyrene sulfonate ( kayexalate ) by mouth or enema to reverse hyperkalemia with mild hyperkalemic symptoms (malaise, loss of appetite, muscle weakness) Hypertonic glucose, insulin, and sodium bicarbonate I.V.— For more severe hyperkalemic symptoms (numbness and tingling and ECG changes) Hemodialysis to correct electrolyte and fluid imbalances Peritoneal dialysis to correct electrolyte and fluid imbalances.

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