Acute kidney failure Rawabi alboqomi

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.

: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 .

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

rise in the creatinine level medications

cimetidine trimethoprim

inhibit the kidney’s tubular secretion of creatinine .

rabdomylisis

rise in the BUN level

can occur from GI or mucosal bleeding

steroid use high protein intake

Symptoms of acute renal failure: Usually asymptomatic Swelling especially of the legs and feet.Oliguria or anurea.

Thirst and a dry mouth.Tachycardia

Dizness

Loss of appetite, nausea , and vomiting .

Feeling confused or sleepy .

Flank pain.

Causes of acute renal failure

:Prerenal failureThe commonest cause of AKF

Reversible Decrease in renal perfusion due to :

Dehydration Diuretic use Poor fluid intake Vomiting Diarrhea

Burns

Continue the causes:

Hemorrhage CHF

Periphral vasodilation : Sepsis Excessive antihypertensive medications Renal arterial obstruction Cirrhosis .. Hepatorenal syndrome

-NSAIDs -ACE inhibitors

-Cyclosporin

Can precipitate prerenal failure

Prerenal AKF is Reversible if blood flow restored

If Hypoperfusion persistence >>> ischemia >>> acute tubular necrosis .

Pathophisiology BLOOD FLOW

GFR LOWDecrease CLEARANCE OF CR – BUN

SO THE LABS WILL SHOW :

Increase urine osmolality Decrease urine NaIncrease urine / plasma Cr ratio > 40 : 1

Increase BUN/Cr ratio > 20 : 1 Oliguria

Intra-renal failure:

Kidney tissue is damged

Glomerular filtration and tubular function are significantly impaired

Intrarenal

Glomerular diseaseTubular disease

Tubular disease

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

Lupus

Glomerular disease

Poststreptococal GNWegeners granulomatosis

goodpastures syndrome

- Vascular disease TTP - HUS

- Interstitial diseasesAllergic interstitial nephritis

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

Postrenal failure : the least common cause

:Causes

Any obstruction below kidney Enlarged prostate

Obstruction of solitary kidney Nephrolithiasis

Obstructing neoplasm in bladder - cervix - prostateRetroperitoneal fibrosis

Three basic tests for postrenal failure:

Physical examination US

foley catheter

Diagnosis:

Blood test Shows :

Elevation in (bun / Cr) levels Electrolytes level Albumin level CBC

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

Fatty casts indicate >> nephrotic syndrome

Urine Na -Cr and osmolality

Urine culture if infection suspected

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

Complicatios :

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

Metabolic

Hyperkalemia

Metabolic acidosis correct with sodium bicarbonate

Hypocalcemia

Hyponatremia

Hyperphosphatemia

Hyperuricemia

Uremia Accumulation of urea in blood Infection in 50- 60 % of cases

Multifactorial but uremia impair immune functions Pneumonia Uti Sepsis

Summary of the Causes:

Prerenal - as an adaptive response to severe volume depletion and hypotension, with structurally intact nephronsIntrinsic - in response to cytotoxic, ischemic, or inflammatory insults to the kidney, with structural and functional damagePostrenal - from obstruction to the passage of urine

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

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

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

Intrarenal

If develop ATN therapy is supportive If oliguric ( furosemide) increase urine flow

Postrenal

Bladder catheter Consider urology consultation

Thank you Have a nice week end