*ACUTE & CHRONIC RENAL FAILURERONI YULIWAR

*ObjectivesUpon completion of this lesson, the student will be able todifferentiate between acute and chronic renal failure.

*BUN & CreatinineEvaluation of Renal FunctionBUN: Blood Urea Nitrogen ( 10 mg/dL )Reflects excretion of UREA Urea is an end product of protein metabolismIs affected by volume status & protein intakeRises when GFR decreases below 40-60%Creatinine: ( 1 mg/ dL )Product of muscle metabolismNot affected by fluid status or diet

*Renal FailureRenal failure results when the kidneys cannot remove the bodys metabolic wastes (urea) or perform their regulatory functions. The wastes accumulate in the body fluids, leading to a disruption in endocrine and metabolic functions as well as fluid, electrolyte, and acidbase disturbances. Renal failure is a systemic disease and is a final common pathway of many different kidney and urinary tract diseases.

*Acute Renal Failure (ARF)Sudden interruption of renal functionCaused by: obstruction, poor circulation, kidney disease or medicationsKidneys are unable to clear fluids & nitrogen waste productsClassified as:PrerenalIntrarenalPostrenal

*Ethiology ARF:Pre RenalPrerenal conditions occur as a result of impaired blood flow that leads to hypoperfusion of the kidney and a drop in the GFR. The causes could be hemorrhage, myocardial infarction, heart failure, or cardiogenic shock, sepsis or anaphylaxis.

*Pre-renal55- 60%Any condition that reduces blood flow to the kidneys ( upstream )Cardiac failureDecreased cardiac outputHypovolemiaBurns, dehydration, trauma, shock, diuretic overusePeripheral vasodilationAntihypertensive medicationsRenal artery stenosis or embolism

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ARFClinical ManifestationsPrerenal:oliguria tachycardiahypotensiondry mucous membraneslethargy progressing to coma

*Ethiology ARF:Intra RenalIntrarenal causes of ARF are the result of actual parenchymal damage to the glomeruli. Conditions such as burns, crush injuries, and infections, nephrotoxic agents (nonsteroidal anti-inflammatory drugs (NSAIDs); angiotensin-converting enzyme (ACE) inhibitors), may lead to acute tubular necrosis and cessation of renal function. With burns and crush injuries, myoglobin (a protein released from muscle when injury occurs) and hemoglobin are liberated, causing renal toxicity, ischemia, or both.

*Intrarenal35 - 40%Filtering structures of the kidneys are damagedUsually from acute tubular necrosis Ischemic damage to tubular cellsNephrotoxic substancesGentamycin, NSAID, Lead, Analgesics, DiureticsRhabdomyolysis: breakdown of muscle myoglobinCaused by major trauma or systemic infectionsAcute glomerularnephritis: inflammation of the nephrons

*Ethiology ARF: Post Renal Postrenal causes of ARF are usually the result of an obstruction somewhere distal to the kidney. Pressure rises in the kidney tubules; eventually, the GFR decreases. Common causes include calculi (stones), tumors, benign prostatic hyperplasia, strictures, and blood clots.

*ARFClinical ManifestationsIntrarenal:Uremia: build up of urea (nitrogenous wastes)confusionaltered peripheral sensation fluid shift to lungsinfection due to decreased cell mediated immunityelectrolyte imbalancesacidosis ( H+ ions are not secreted )

*Post-renal

*Pathophysiology:Acute Renal Failure (ARF)Acute renal failure (ARF) is a sudden and almost complete loss of kidney function over a period of hours to days. ARF manifests with oliguria (less than 400 mL/day of urine), anuria (less than 50 mL/day of urine), or normal urine volume. The patient has high serum creatinine and BUN levels (azotemia) and retention of other metabolic waste products normally excreted by the kidneys.

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ARFPathophysiologyOliguric Phase: less than 400mL / 24 hoursAt risk for fluid volume excessAzotemia: elevated BUN, Creatinine and Uric Aciddecreased level of consciousnessElectrolyte imbalance: hyperkalemiaRenal cells can regenerate if etiology is treated

*ARFPathophysiologyDiuretic Phase: those who recover renal functiongradual increase in urine outputtubular transport is still hinderedurine is dilutehigh urinary outputs places pt at risk for dehydrationRecovery Phase: gradual return to normal function3 to 12 months or longer for recovery

*Comparing Types of Acute Renal FailureTYPES

*CHRONIC RENAL FAILURE (CRF)Progressive & irreversible loss of nephrons24 hour creatinine clearance: most accurate measurement of GFRserum creatinine is compared to urine creatininemay have very high creatinine levels d/t ability to compensate initially Changes in erythropoetin production 10-15% renal functionrequires dialysis graft or shunt Anuria:

*CLINICAL MANIFESTATIONSAlmost every system of the body is affected when there is failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic with persistent nausea, vomiting and diarrhea. The skin and mucous membranes are dry from dehydration, and the breath may have the odor of urine. Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures..

*ReferencesHansen, M. (1998). Pathophysiology: Foundations of disease and clinical intervention. Philadelphia: Saunders.Huether, S. E., & McCance, K. L. (2002). Pathophysiology. St. Louis: Mosby.http://www.pathoplus.com

*****Our kidneys are highly vascular organs and receive 1-1.2 L of blood/minute (20-25% of our cardiac output)

The GFR is the filtration of the plasma per unit of time = directly r/t perfusion pressure of glomerular capillaries. It reflects the function of the renal tissue.

Pre-renal = anything that reduces the blood flow to the kidneysIntra-renal= inside the kidney structure there is damage of some sortPost-renal= there is something obstructing the outflow (e.g. kidney stone)

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