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Acute kidney failure Rawabi alboqomi. This lecture was conducted during the Nephrology Unit Grand Ground by a Sub-intern under Nephrology Division, Department.

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Presentation on theme: "Acute kidney failure Rawabi alboqomi. This lecture was conducted during the Nephrology Unit Grand Ground by a Sub-intern under Nephrology Division, Department."— Presentation transcript:

1 Acute kidney failure Rawabi alboqomi

2 This lecture was conducted during the Nephrology Unit Grand Ground by a Sub-intern under Nephrology Division, Department of Medicine in King Saud University. Nephrology Division is NOT responsible for the content of the presentation for it is intended for learning and /or education purpose only.

3 :Definition Of Acute Renal Failure an abrupt or rapid decline in renal filtration function. This condition is usually marked by : azotemia a rise in serum creatinine concentration and a rise in [BUN] concentration.

4 Serum creatinine Normal level.5 – 1 mg/dl (45-90 micromol/ L ) in women.7 – 1.2 mg / dl (60 – 110 micro mol /L )in men BUN Normal level 7 – 21 mg /dl

5 rise in the creatinine level medications cimetidine trimethoprim inhibit the kidney’s tubular secretion of creatinine. rabdomylisis

6 rise in the BUN level can occur from GI or mucosal bleeding steroid use high protein intake

7 Symptoms of acute renal failure : Usually asymptomatic Swelling especially of the legs and feet. Oliguria or anurea. Thirst and a dry mouth. Tachycardia

8 Dizness Loss of appetite, nausea, and vomiting. Feeling confused or sleepy. Flank pain.

9 Causes of acute renal failure

10 :Prerenal failure The commonest cause of AKF Reversible Decrease in renal perfusion due to : Dehydration Diuretic use Poor fluid intake Vomiting Diarrhea Burns

11 Continue the causes : Hemorrhage CHF Periphral vasodilation : Sepsis Excessive antihypertensive medications Renal arterial obstruction Cirrhosis.. Hepatorenal syndrome

12 - NSAIDs - ACE inhibitors - Cyclosporin Can precipitate prerenal failure

13 Prerenal AKF is Reversible if blood flow restored If Hypoperfusion persistence >>> ischemia >>> acute tubular necrosis.

14 Pathophisiology BLOOD FLOW GFR LOW Decrease CLEARANCE OF CR – BUN SO THE LABS WILL SHOW : Increase urine osmolality Decrease urine Na Increase urine / plasma Cr ratio > 40 : 1

15 Increase BUN/Cr ratio > 20 : 1 Oliguria

16 Intra-renal failure : Kidney tissue is damged Glomerular filtration and tubular function are significantly impaired

17 Intrarenal Glomerular diseaseTubular disease

18 NSAIDs Chemotherapy as cisplatin Hemoglobinuria Poisons Myoglobinurea Radiocontrast agents Antibiotics as aminoglycoside Lupus

19 Glomerular disease Poststreptococal GN Wegeners granulomatosis goodpastures syndrome - Vascular disease TTP - HUS - Interstitial diseases Allergic interstitial nephritis

20 Symptoms depend on the cause : Edema usually present Recovery take longer than in prerenal failure Labs shows Decrease Bun /Cr ratio <20:1 Increase urine Na Decrease urine osmolality Decrease urine plasma Cr ratio < 20:1

21 Postrenal failure : the least common cause :Causes Any obstruction below kidney Enlarged prostate Obstruction of solitary kidney Nephrolithiasis Obstructing neoplasm in bladder - cervix - prostate Retroperitoneal fibrosis

22 Three basic tests for postrenal failure : Physical examination US foley catheter

23 Diagnosis : Blood test Shows: Elevation in (bun / Cr) levels Electrolytes level Albumin level CBC

24 Urine analysis Dipstick test for protein Microscopic examination of urine sediment Hyaline casts in >>> prerenal failure RBC casts >>> glomerular disease WBC casts indicate >>>renal paren chymal inflammation

25 Fatty casts indicate >> nephrotic syndrome Urine Na -Cr and osmolality Urine culture if infection suspected

26 Renal ultrasound : Evaluate kidney size Urinary tract obstruction CT scan : abdomen and pelvis Renal biopsy: Suspicion of acute GN or acute allergic interstitial nephritis Renal arteriography : for renal artery occlusion

27 Complicatios : volume expansion and pulmonary edema >> diuretic (furosemide ) if no response in 2 h >> dialysis

28 Metabolic Hyperkalemia Metabolic acidosis correct with sodium bicarbonate Hypocalcemia Hyponatremia Hyperphosphatemia Hyperuricemia

29 Uremia Accumulation of urea in blood Infection in 50- 60 % of cases Multifactorial but uremia impair immune functions Pneumonia Uti Sepsis

30 Summary of the Causes : Prerenal - as an adaptive response to severe volume depletion and hypotension, with structurally intact nephrons Intrinsic - in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damage Postrenal - from obstruction to the passage of urine

31 Treatment : General measures Avoid medication that decrease renal blood flow As NSAID Also avoid nephrotoxic as aminoglycoside or radiocontrast agents Adjust medication to level of renal function Correct fluid imbalance Diuretics if overloaded Iv if volume depleted

32 Monitor fluid balance by Weight measurements Urine output record Optimize cardiac output BP SHOULD BE 120-140/80-90 Order dialysis if symptomatic uremia Hyperkalemia Volume overload that will not go down by antiduretics

33 Continue treatment Prerenal : Treat the underlying disorder Give NS Eliminate any offending agents (ACE inhibitors – NSAIDs ) If the patient is unstable>> swan ganz monitoring for intravascular volume

34 Intrarenal If develop ATN therapy is supportive If oliguric ( furosemide) increase urine flow Postrenal Bladder catheter Consider urology consultation

35 Thank you Have a nice week end


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