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Acute kidney injury Yousaf khan Lecturer Renal dialysis IPMS- KMU

Acute kidney injury

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Page 1: Acute kidney injury

Acute kidney injuryYousaf khan Lecturer Renal dialysis IPMS- KMU

Page 2: Acute kidney injury

Acute kidney injury Acute renal failure (ARF) Abrupt loss of Kidney function that develops within 7 days. Increase in serum creatinine

AKI may lead to a number of complications, metabolic acidosis high potassium levels Uremia changes in body fluid balance Effects on other organ systems including death People who have experienced AKI may have an increased

risk of chronic kidney disease in the future.

Page 3: Acute kidney injury

Diagnostic ApproachTime of onset – prior serum

creatinineCareful review of history and

physical exam◦Comorbidities◦Medications◦Current illness (vomiting, diarrhea,

blood loss, etc)◦BP, volume status, skin lesions,

flank/abdominal signs

Page 4: Acute kidney injury

Signs and symptomsAccumulation of urea and other nitrogen-

containing substances in the bloodstream lead toFatigueloss of appetiteHeadacheNauseaVomiting Marked increases in the potassium level can lead

to irregularities in the heartbeat, which can be severe and life-threatening

Fluid balance is frequently affected, though blood pressure can be high, low or normal

Page 5: Acute kidney injury

Stages of acute injury

Page 6: Acute kidney injury

Consistent Risk FactorsAgeHypovolemiaHypotensionSepsisCKDHepatic dysfunctionCardiac dysfunctionDMExposure to nephrotoxins

Page 7: Acute kidney injury

Differential Diagnosis of AKIPre-renal

Renal

Post-renal

Page 8: Acute kidney injury

Prerenal Decrease effective blood flow to the kidney low blood volume low blood pressure heart failure liver cirrhosis renal artery stenosis renal vein thrombosis Renal ischaemia can result in depression of GFR inadequate cardiac output

Page 9: Acute kidney injury

IntrinsicGlomerular

◦ Rapidly progressive GN, post-strep GN,

Interstitial nephritis◦ Infection-related, inlammation, drug-induced,

infiltrative (lymphoma, leukemia, sarcoidosis)

Tubular Lesions◦ Post-ishemia, nephrotoxic (drugs, contrast,

anesthetics, heavy metals), pigment nephropathy, light chain, hypercalcemia

Page 10: Acute kidney injury

PostrenalBladder flow obstruction

◦Urethral, bladder neck (BPH), neurogenic bladder

Ureteral obstruction (bilateral or single kidney)◦Stones, clots, tumours, papillary

necrosis, retroperitoneal fibrosis, surgical ligation

Page 11: Acute kidney injury

Urine Output and AKIAnuric

◦< 100 cc / 24 hrsOliguric

◦< 300 cc / 24 hrsNon-olguric

◦Normal urine output, but inadequate clearance

◦GFR 2 ml/min will produce ~3L of urine/day if there is no tubular reabsorption

Page 12: Acute kidney injury

DiagnosisClinical history Urea and creatinine Urine sediment analysisrenal ultrasoundrenal biopsyIndications for renal biopsy in the setting of AKI

includeUnexplained AKI, in a patient with two non-

obstructed normal sized kidneysAKI in the presence of the nephritic syndromeSystemic disease associated with AKIRenal transplant dysfunction

Page 13: Acute kidney injury

Principles of AKI ManagementIdentify AKIAvoid further nephrotoxic injuryOptimize renal hemodynamicsTreat complications

◦ Fluid balance, electrolytes, uremiaNutritional supportRenal Support (RRT)Monitoring after AKI

Page 14: Acute kidney injury

Treatment Identification and treatment of the underlying cause. (1) to prevent cardiovascular collapse and death (2) to call for specialist advice.

In addition to treatment of the underlying disorder, management of AKI routinely includes the avoidance of substances that are toxic to the kidneys, called nephrotoxins. These include NSAIDs such as ibuprofen, iodinated contrasts such as those used for CT scans, many antibiotics such as gentamicin, and a range of other substances

Monitoring of renal function, by serial serum creatinine measurements and monitoring of urine output, is routinely performed. In the hospital, insertion of a urinary catheter helps monitor urine output and relieves possible bladder outlet obstruction, such as with an enlarged prostate.

Page 15: Acute kidney injury

Specific therapies In prerenal AKI without fluid overload administration of intravenous fluids is typically the first step to

improve renal function.

Volume status may be monitored with the use of a central venous catheter to avoid over- or under-replacement of fluid.

Should low blood pressure prove a persistent problem in the fluid-replete patient, inotropes such as norepinephrine and dobutamine may be given to improve cardiac output and hence renal perfusion.

Intrinsic AKI require specific therapies.

If the cause is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary.

Page 16: Acute kidney injury

Renal replacement therapyRenal replacement therapy such

as withHemodialysisPeritoneal dialysisCRRT

Page 17: Acute kidney injury

Thank you