ACUTE RENAL FAILURE (ARF) GAGAL GINJAL AKUT By: Jessica, sumber: Harrison, Smith Urology, kapita selekta DEFINISI

Acute renal failure (ARF) is a syndrome characterized by rapid decline in glomerular filtration rate (hours to days), retention of nitrogenous waste products, and perturbation of extracellular fluid volume and electrolyte and acid-base homeostasis. Gagal ginjal akut adalah penurunan fungsi ginjal secara tiba-tiba yang biasanya, tapi tidak seluruhnya, reversibel. JENIS-JENIS ARF (1) diseases that cause renal hypoperfusion without compromising the integrity of renal parenchyma (prerenal ARF, prerenal azotemia) (~55%); (2) diseases that directly involve renal parenchyma(intrinsic renal ARF, renal azotemia) (~40%) (3)diseases associated with urinary tract obstruction (postrenal ARF, postrenal azotemia) (~5%). ETIOLOGI Prerenal ARF : praginjal atau sirkulasi, terjadi akibat kurangnya perfusi ginjal. I. Hypovolemia A. Hemorrhage, burns, dehydration B. Gastrointestinal fluid loss: vomiting, surgical drainage, diarrhea C. Renal fluid loss: diuretics, osmotic diuresis (e.g., diabetes mellitus), hypoadrenalism D. Sequestration in extravascular space: pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia II. Low cardiac output A. Diseases of myocardium, valves, and pericardium; arrhythmias; tamponade B. Other: pulmonary hypertension, massive pulmonary embolus, positive pressure mechanical ventilation III. Altered renal systemic vascular resistance ratio A. Systemic vasodilatation: sepsis, antihypertensives, afterload reducers, anesthesia, anaphylaxis B. Renal vasoconstriction: hypercalcemia, norepinephrine, epinephrine, cyclosporine, tacrolimus, amphotericin B C. Cirrhosis with ascites (hepatorenal syndrome) IV. Renal hypoperfusion with impairment of renal autoregulatory responses Cyclooxygenase inhibitors, angiotensinconverting enzyme inhibitors V. Hyperviscosity syndrome (rare) Multiple myeloma, macroglobulinemia, polycythemia Intrinsic Renal ARF: akibat penyakit pada ginjal atau pembuluhnya, terdapat kelainan histologi. I. Renovascular obstruction (bilateral or unilateral in the setting of one functioning kidney) A. Renal artery obstruction: atherosclerotic plaque, thrombosis, embolism, dissecting aneurysm, vasculitis B. Renal vein obstruction: thrombosis, compression II. Disease of glomeruli or renal microvasculature A. Glomerulonephritis and vasculitis B. Hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, toxemia of pregnancy, accelerated hypertension, radiation nephritis, systemic lupus erythematosus, scleroderma III. Acute tubular necrosis A. Ischemia: as for prerenal ARF (hypovolemia, low cardiac output, renal vasoconstriction, systemic vasodilatation), obstetric complications (abruption placentae, postpartum hemorrhage) B. Toxins 1.Exogenous: radiocontrast, cyclosporine, antibiotics (e.g., aminoglycosides), chemotherapy (e.g., cisplatin), organic solvents (e.g., ethylene glycol), acetaminophen, illegal abortifacients 2. Endogenous: rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (e.g., myeloma) IV. Interstitial nephritis A. Allergic: antibiotics (e.g., -lactams, sulfonamides, trimethoprim, rifampicin), nonsteroidal anti-inflammatory agents, diuretics, captopril B. Infection: bacterial (e.g., acute pyelonephritis, leptospirosis), viral (e.g., cytomegalovirus), fungal (e.g., candidiasis) C. Infiltration: lymphoma, leukemia, sarcoidosis D. Idiopathic

In addition. renal pelvis. cellular debris. Bladder neck Neurogenic bladder. sulphonamides VI. During the early stages of obstruction (hours to days). and ifosfamide. cyclosporine. Ureteric Calculi. acyclovir. Hence. and tacrolimus (FK506). predominantly by inducing intrarenal vasoconstriction. particularly in hypovolemic or acidotic individuals. Leukocyte accumulation is frequently observed in vasa recta. but arteriolar vasoconstriction soon supervenes. congenital valve. and chemotherapeutic agents. carboplatin. The gold standard is the response to appropriate fluid repletion. Postrenal ARF Because one kidney has sufficient clearance capacity to excrete the nitrogenous waste products generated daily. and calyces and a fall in GFR. Microscopy of the urinary sediment is usually bland. methotrexate. is the major trigger for ARF in patients with multiple myeloma (myeloma cast nephropathy). which mediates water reabsorption. bilateral ureteric obstruction. ARF from obstruction requires obstruction to urine flow between the external urethral meatus and bladder neck. These are adaptive responses of the kidney directed to maintain the GFR. blood clot III. such as cisplatin. As a result there is gradual distention of the proximal ureter. oxalate. such as acyclovir. Renal hypoperfusion stimulates both the sympathetic nervous system and the renin-angiotensin system to cause renal vasoconstriction and sodium avidity. The pathophysiology of prerenal azotemia relates to the reduction in RBF. Intratubular deposition and obstruction Myeloma proteins. urate. . Renal allograft rejection Postrenal ARF (Obstruction) : terjadi akibat obstruksi aliran urin.V. and pentamidine. calculi. cancer. or unilateral ureteric obstruction in a patient with one functioning kidney or with preexisting chronic renal insufficiency. Furthermore. Necrosis is most severe in the straight portion (pars recta) of proximal tubules but may also affect the medullary thick ascending limb of the loop of Henle. Hypercalcemia can compromise GFR.g. Both rhabdomyolysis and hemolysis can induce ARF. PATHOLOGY OF ISCHEMIC AND NEPHROTOXIC ARF The classic pathologic features of ischemic ARF are patchy and focal necrosis of tubule epithelium with detachment from its basement membrane and occlusion of tubule lumens with casts composed of intact or degenerating epithelial cells. Direct toxicity to tubule epithelial cells and/or intratubular obstruction are major pathophysiologic events in ARF induced by many antibiotics and anticancer drugs. The hallmark of prerenal azotemia is its reversibility with treatment of the underlying cause and the lack of structural damage to the kidney. however. and myeloma light chains. foscarnet. Tamm-Horsfall mucoprotein. (Skema di halaman paling belakang) Nephrotoxicity ARF Intrarenal vasoconstriction is a pivotal event in ARF that is triggered by radiocontrast agents (contrast nephropathy). Urethra Stricture. The formation of intratubular casts containing filtered immunoglobulin light chains and other proteins. by promoting intrarenal oxidative stress and by inducing intratubular cast formation. cancer. amphotericin B. In addition. Myoglobin and hemoglobin or other compounds released from muscle or red blood cells cause ARF via toxic effects on tubule epithelial cells. continued glomerular filtration leads to increased intraluminal pressure upstream to the site of obstruction.. including Tamm-Horsfall protein produced by thick ascending limb cells. urine production in prerenal ARF is characterized by low volume. hemoglobin. Frequent offenders are the antimicrobial agents. uric acid. The most common endogenous nephrotoxins are calcium. prostatic hypertrophy. hypotension is a powerful stimulus to the release of an antidiuretic hormone. and pigments. external compression (e. and a high urine osmolality. increased urinary excretion of creatinine. decreased concentration of urinary sodium. leading to a further decline in glomerular filtration. blood clot. the morphology of the glomeruli and renal vasculature is characteristically normal. The return of renal function to the previous baseline within 24 to 72 hours is usually considered to indicate prerenal disease. both hemoglobin and myoglobin are potent inhibitors of nitric oxide bioactivity and may trigger intrarenal vasoconstriction and ischemia in patients with borderline renal hypoperfusion. myoglobin. phimosis PATOFISIOLOGI Prerenal ARF Prerenal ARF is caused by transient renal hypoperfusion that may induce a fall in the GFR and produce urinary sodium avidity. retroperitoneal fibrosis) II. sloughed papillae. aminoglycosides. Acute obstruction is initially associated with modest increase in renal blood flow. oxalate. I. light chains are directly toxic to tubule epithelial cells.

retinopathy. cardiac failure. thrombocytopenia. 2.g. UNa >20 mmol/L. ARF mediated by ischemia or toxins (ATN) 1. hypocomplementemia. new cardiac murmur. sinusitis. Urinalysis: Proteinuria. Additional exam: Inferior vena cavagram and selective renal venogram. Urinalysis: Muddy brown granular or tubular epithelial cell casts. Additional exam: Elevated LDH with normal transaminases. renal biopsy 3. epithelial cell casts. hypertension. Urinalysis: Mild proteinuria. Urinalysis: Red cells. recent infection). recent manipulation of aorta. B. low jugular venous pressure. history of hepatitis B or C infection. ecchymoses. fever. schistocytes on blood smear. cyclosporine. proteinuria. Additional exam: Eosinophilia. hypotension (e. SG <1. blood cultures. Atheroembolism Age usually>50 years. MANIFESTASI KLINIS DAN CARA MENDIAGNOSIS Prerenal ARF Clinical Feature: Evidence of true volume depletion (thirst. FENa >1%. increased LDH. ANA. Hemolytic-uremic syndrome/thrombotic thrombocytopenic purpura Compatible clinical history (e. red cells.In nephrotoxic ARF. Tubule cell necrosis is less pronounced than in ischemic ARF. morphologic changes tend to be most prominent in both the convoluted and straight portions of proximal tubules.. treatment with NSAIDs or ACE inhibitors.g. red cell casts. Diseases involving large renal vessels 1. Additional exam: Low C3. Additional exam: Anemia. papilledema. sepsis. mild proteinuria. Additional exam: LVH by echocardiography/ECG. rapid resolution of ARF upon restoration of renal perfusion. ASO. weight loss. rarely casts. fluid output > input) or decreased “effective” circulatory volume (e. neurologic dysfunction. anti-GBM Ab. occasionally red cells.. renal arteriogram 2. Malignant hypertension Severe hypertension with headaches. Ischemia Recent hemorrhage. rarely red cell/ granular casts.. C. cardiac arrest). Glomerulonephritis/vasculitis Compatible clinical history (e. FENa <1%. flank pain. Diseases of small vessels and glomeruli 1. neurologic abnormalities. retinal plaques. Exogenous toxins Recent radiocontrast study. mild proteinuria. flank or abdominal pain. eosinophiluria.015 2. pallor. surgery. heart failure. dysmorphic red cells. skin rash or ulcers. Intrinsic Renal ARF A.015 3. renal biopsy. liver failure).018. livedo reticularis. Urinalysis: Muddy brown granular or tubular. UNa <10 mmol/L. urine osmolality >600 mOsm/kg Some Confirmatory Tests Occasionally requires invasive hemodynamic monitoring. cryoglobulins. recent gastrointestinal infection. ANCA. Renal vein thrombosis Evidence of nephrotic syndrome or pulmonary embolism. Urinalysis: May be normal. subcutaneous nodules. anti-DNase. lung hemorrhage. skin biopsy. postural or absolute hypotension and tachycardia. Endogenous toxins . Typical Urinalysis: Hyaline casts. SG <1. anticoagulation. anovulants).. nephrotoxic antibiotics or anticancer agents often coexistent with volume depletion. hematuria. 3. resolution of ARF with control of blood pressure. dry mucous membranes/axillae. altered red cell morphologic structure in peripheral blood smears.g. Urinalysis: Often normal. vasculopathy. UNa >20 mmol/L. or chronic renal insufficiency. Renal artery thrombosis History of atrial fibrillation or recent myocardial infarct. Urinalysis: Red cell or granular casts. FENa >1%. SG >1. arthralgias.g. palpable purpura. white cells. renal biopsy.

white cells (frequently eosinophiluria). Additional exam: Hyperkalemia. Severe hypovolemia due to hemorrhage should be corrected with packed red cells. osmolal gap (for ethylene glycol). Acute bilateral pyelonephritis Flank pain and tenderness. hyperuricemia. and fever. acidosis. hyperphosphatemia. Urinalysis: Urine supernatant pink and positive for heme. hyperkalemia. renal ultrasound. IVP. complement component. palpable bladder. myeloma (bone pain). hypocalcemia. and uric acid. red cells. electrocardiogram. antistreptolysin O. renal biopsy 2.. hyperphosphatemia (for tumor lysis). Note: UNa. Allergic interstitial nephritis Recent ingestion of drug. rash. urine sodium concentration. Urinalysis: Frequently normal. Additional exam: Systemic eosinophilia. proteinuria (occasionally nephrotic). rarely red cell casts. proteinuria. . antinuclear antibody. computed tomography. left ventricular hypertrophy. Additional exam: Hyperkalemia. malignancy.g. ANCA. CPK (MM). pancreatitis). lactate dehydrogenase. LDH. burns. CT. pink plasma positive for hemoglobin. toxic. Postrenal ARF Abdominal or flank pain. ECG. or ethylene glycol ingestion. Additional exam: Hyperuricemia. or arthralgias. Urinalysis: Leukocytes. CT scan.History suggestive of rhabdomyolysis (seizures. Urinalysis: Urine supernatant positive for heme.010 Urine osmolality (mOsm/kgH2O) >500 ~300 Plasma BUN/creatinin ratio >20 <10-15 Renal failure indexa <1 >1 UNa x PCr/UCr Urinary sediment Hyaline cast Muddy brown granular cast PENATALAKSANAAN DAN PENCEGAHAN Prerenal ARF The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia must be tailored according to the composition of the lost fluid. circulating or urinary monoclonal spike (for myeloma). red cells. trauma). ANA. Urinalysis: Urate crystals. anti-glomerular basement membrane antibody. increased circulating myoglobin. SG. or prostatic hypertrophy. Additional exam: Urine and blood cultures. LVH. Acute diseases of the tubulointersitium 1. hematuria if stones. IVP. ethanol abuse. whereas isotonic saline is usually appropriate replacement for mild to moderate hemorrhage or plasma loss (e. bacteria. skin biopsy of rash (leukocytoclastic vasculitis). respectively. Urinalysis: White cell casts. CK. hemorrhage. Additional exam: Plain film. hypocalcemia. anti-GBM Ab. ASO. hyperphosphatemia. History suggestive of hemolysis (blood transfusion). creatine kinase. specific gravity. coma. dipstick-negative proteinuria. intravenous pyelogram. C3. antineutrophil cytoplasmic autoantibody. toxicology screen.020 ~1. D. oxalate crystals. febrile. Urine Diagnostic Indices in Differentiation of Prerenal versus Intrinsic Renal ARF Diagnostic Index Prerenal Intrinsic Renal Fractional excretion of sodium (%)a <1 >1 UNa x PCr/(PNa x UCr)x 100 Urine sodium concentration (mmol/L) <10 >20 Urine creatinine to plasma creatinine ratio >40 <20 Urine urea nitrogen to plasma urea >8 <3 nitrogen ratio Urine specific gravity >1. retrograde or anterograde pyelography. History suggestive of tumor lysis (recent chemotherapy).

sloughed papilla) or bypassed by insertion of a ureteric stent (e. depending on the primary pathology. The continuous dialysis techniques allow for easier management in many hemodynamically unstable patients in intensive care units.. calculus. potassium-binding ion-exchange resins (e. MANAGEMENT OF ISCHEMIC AND NEPHROTOXIC ACUTE RENAL FAILURE MANAGEMENT ISSUE THERAPY REVERSE CAUSATIVE RENAL INSULT Ischemic ARF: Restore systemic hemodynamics and renal perfusion Nephrotoxic ARF: Eliminate nephrotoxins. toxemia of pregnancy. Peritoneal dialysis or hemodialysis should be used as necessary to avoid or correct uremia. Hyponatremia: restriction of enteral free water intake (<1 L/d). Postrenal ARF Obstruction of the urethra or bladder neck is usually managed initially by transurethral or suprapubic placement of a bladder catheter. Dopamine.. or fluid overload. which provides temporary relief while the obstructing lesion is identified and treated definitively. Higher doses of 5–20 μg/kg may be necessary if systemic hypotension persists after volume correction. 0. eliminate K+ supplements and K+-sparing diuretics. diuretics (usually loop blockers ± thiazide).2). ureteric obstruction may be treated initially by percutaneous catheterization of the dilated renal pelvis or ureter. chelators PREVENTION AND TREATMENT OF COMPLICATIONS Intravascular volume overload: Salt (1–2 g/d) and water (usually <1 L/d) restriction.g.Hypotonic solutions (e. sodium bicarbonate (usually 50–100 mmol).g. calcium gluconate (10 mL of 10% solution over 5 min). enteral or parenteral nutrition (if recovery prolonged or patient very catabolic) . aluminum hydroxide) Hypocalcemia: Calcium carbonate (if symptomatic or if sodium bicarbonate to be administered). (2) Kayexalate. Intrinsic Renal ARF ARF due to other intrinsic renal diseases such as acute glomerulonephritis or vasculitis may respond to glucocorticoids.g.6 g/kg per day). obstructing lesions can often be removed percutaneously (e. phosphate binding agents (calcium carbonate.g. consider specific measures (e.. Indeed. may increase renal blood flow without systemic pressor responses. dialysis Hyperphosphatemia: restriction of dietary phosphate intake (usually <800 mg/d). Hemodialysis in patients with acute renal failure can be either intermittent or continuous (with arteriovenous or venovenous hemofiltration techniques). sodium bicarbonate (maintain serum bicarbonate >15 mmol/L or arterial pH >7. avoid hypotonic intravenous solutions (including dextrose solutions).45% saline) are usually recommended as initial replacement in patients with pre renal ARF due to increased urinary or gastrointestinal fluid losses.g. Cardiac failure may require aggressive management with positive inotropes..6 g/kg per day of high biologic value). Vascular access is obtained with percutaneous catheters. glucose (50 mL of 50% dextrose) and insulin (10 units regular). Hyperkalemia: Restriction of dietary K+ intake (usually <40mmol/d). Aggressive control of systemic arterial pressure is of paramount importance in limiting renal injury in malignant hypertensive nephrosclerosis. and other vascular diseases. Similarly. With appropriate regulation of the volume of fluid administered.. antiarrhythmic drugs. and potassium and bicarbonate supplemented as appropriate. 25–50 g (with sorbitol) orally or by enema. sodium polystyrene sulphonate). Hypertension and ARF due to scleroderma may be exquisitely sensitive to treatment with ACE inhibitors. solutions of glucose and essential amino acids to provide 30–35 kcal/kg are used to correct or reduce the severity of the catabolic state accompanying acute tubular necrosis. If oliguria and hypotension persist in a well-hydrated patient. This condition can be treated with (1) intravenous sodium bicarbonate administration. calcium gluconate (10–20 mL of 10% solution) Hypermagnesemia: discontinue Mg2+-containing antacids Hyperuricemia: treatment usually not necessary [if <890 μmol/L (<15 mg/dL)] Nutrition: restriction of dietary protein (~0. carcinoma). Serum potassium and acid-base status should be monitored carefully. 1–5 μg/kg/min. Pressor agents that restore systemic blood pressure while maintaining renal blood flow and renal function are most useful. dialysis (with low K+-dialysate) Metabolic acidosis: Restriction of dietary protein (usually 0. and (4) intravenous calcium preparations to prevent cardiac irritability. preload and afterload reducing agents. forced alkaline diuresis. (3) intravenous glucose and insulin. and mechanical aids such as intraaortic balloon pumps. carbohydrate (~100 g/d). alkylating agents. Glucocorticoids also hasten remission in some cases of allergic interstitial nephritis. Serum potassium must be closely monitored to ensure early recognition of hyperkalemia. and/or plasmapheresis. ultrafiltration or dialysis. vasopressor drugs are indicated in an effort to correct the hypotension associated with sepsis or cardiogenic shock. hypokalemia.

Kelainan ginjal. KOMPLIKASI • Expansion of ECF volume • Gangguan elektrolit: hyperkalemia. kejang • Gastrointestinal: nausea. Penatalaksanaan gagal ginjal a. mild gastrointestinal bleeding • Uremic syndrome • Vigorous diuresis and hypernatremia (during recovery phase) • Infection: pneumonia. nosocomial infection. Bila perlu dilakukan USG ginjal. Mencegah dan memperbaiki perdarahan saluran cerna. keseimbangan cairan. c. 2. ulkus peptikum. hyperkalemia or severe acidosis resistant to conservative measures. Feses diperiksa untuk adanya perdarahan dan dapat dilakukan endoskopi. intractable intravascular volume overload. Dialisis dini atau hemofiltrasi sebaiknya tidak ditunda sampai ureum tinggi. disertai penurunan Hb.V. and pulmonary embolism • Neurologi: iritabilitas neuromuscular. pericarditis and pericardial effusion. hiperkalemia. pulmonary edema. gangguan miksi. atau terjadi kelebihan cairan. f. arteriografi. ACE inhibitors. Continuous haemofiltration dan dialisis peritoneal paling baik dipakai di ruang intensif. d. c. PROGNOSIS The mortality rate among patients with ARF approximates 50%. Oliguria (<400 mL/d) at time of presentation and a rise in serum creatinine of >265 μmol/L (>3 mg/dL) are associated with a poor . Dilakukan perbaikan asidosis. koma. Biasanya antagonis histamin H2 (misalnya ranitidin) diberikan pada pasien sebagai profilaksis. hypocalcemia • Hematologi: anemia. Periksa konsentrasi natrium urin. Diagnosa dan tatalaksana penyebab a. b. pada kedaruratan jantung dan dialisis. gangguan kesadaran. atau nyeri pinggang. tremor. metabolic acidosis. sepsis. dam status dehidrasi. Summary of Management (source: Kapita Selekta) 1. mikroskopik urin. Mencegah dan memperbaiki infeksi. diberikan diuretik. Dilakukan pengkajian klinis. pemberian Ca I. sedangkan hemodialisis intermiten dengan kateter subklavia ditujukan untuk pasien lain dan sebagai tambahan untuk pasien katabolik yang tidak adekuat dengan dialisis peritoneal atau hemofiltrasi. prophylactic dialysis when urea >100–150 mg/dL or creatinine >8–10 mg/dL PRESCRIBING OF MEDICATIONS Choice of agents: avoid other nephrotoxins. selain untuk mengetahui adanya obstruksi juga untuk pengawasan akurat dari urin dan mengambil bahan pemeriksaan.V. Dilakukan pengkajian klinis meliputi apakah kandung kemih penuh. myocardial infarction. pemberian glukosa dan insulin I. Mencapai dan mempertahankan keseimbangan Na dan air. cyclooxygenase inhibitors. volume darah dikoreksi. flap. bisa melalui suplemen tinggi kalori atau hiperalimentasi I. Memberikan nutrisi yang cukup. terutama ditujukan terhadap infeksi saluran napas dan nosokomial. muntah. Kelainan praginjal. Dapat pula dideteksi dari kenaikan rasio ureum/kreatinin. Dicoba memasang kateter urin.V. Drug dosing: adjust doses and frequency of administration for degree of renal impairment. e.. Masukan Na diabatasi hingga 60 mmol/hari dan cairan cukup 500 ml/hari di luar kekurangan hari sebelumnya atau 30 ml/jam di luar jumlah urin yang dikeluarkan jam sebelumnya. atau tes lainnya. ada pembesaran prostat. Dilakukan pengkajian klinis meliputi factor pencetus. Mencegah dan memperbaiki hiperkalemia.Indications for dialysis: clinical evidence (symptoms or signs) of uremia. gastritis. urinalisa. and ~60% following trauma or major surgery. Kateter harus segera dilepas bila diagnosis obstruksi kandung kemih dapat disingkirkan. pertimbangkan kemungkiann biopsi ginjal. ~30% in toxin-related ARF. dipertimbangkan pemberian inotropik. Kelainan pascaginjal. and radiocontrast unless absolute indication and no alternative agent. mortality rates vary greatly depending on the cause of ARF: ~15% in obstetric patients. b. Ureum tidak boleh melebihi 30-40 mmol/L. diatesis hemoragik • Cardiopulmonary complications: arrhythmias. dan dopamin. mild hyperphosphatemia. Demam harus segera dideteksi dan diterapi.

.prognosis and probably reflect the severity of renal injury and of the primary illness. Mortality rates are higher in older debilitated patients and in those with multiple organ failure.

PATOFISIOLOGI PRERENAL DAN ISCHEMIC ARF ↓ true or effective circulatory volume Activation of central baroreceptor Angiotensin II Norepinephrine AVP Prerenal ARF or initiation phase of ischemic ARF Preferential constriction afferent arteriole PG synthesis Autoregulation Vasoconstriction/mesangial cell contraction (-) Reduced renal blood flow and GFR If hypoperfusion sufficient to overwhelm renal autoregulatory defenses Ischemic injury to renal parenchyma Endothelial dysfunction Medullary congestion Tubule epithelial cell injury (proximal tubule and thick ascending limb) Persistent medullary ischemia Tubule obstruction Backleak of filtrate Maintenance phase of ischemic ARF Sustained reduction in GFR Recovery of renal perfusion Regeneration of tubule epithelium Recovery phase of ischemic ARF Recovery of GFR .

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