PATHOPHYSIOLOGYOF ACUTE RENAL FAILURE

Bayu F. Wibowo

Bag. Ilmu Bedah FK UNAND

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 (-) End-stage renal disease, prerenal azotemia, and death.

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).

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

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

Bladder Obstruction

Ureteral Obstruction

Urethral Obstruction

Postrenal Failure

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

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

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

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.

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.

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.

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

Complications

Chronic Renal Failure

Ischemic Parenchymal Injury

Intrinsic Renal Azotemia

Electrolyte Imbalance

Metabolic Acidosis

Pulmonary Edema

Hypertensive Crisis

Infection

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

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.