ACUTE RENAL FAILURE

Acute renal failure (ARF) is sudden decrease of renal function, manifesting with the progressive azotemia caused by the accumulation of the nitrogenous end-products of metabolism accompanied by a wide range of other disturbances, including metabolic derangements such as metabolic acidosis and hyperkalemia, disturbances of body fluid balance, and effects on many other organ systems

4-5% of hospital admissions to a general medical/surgical ward will go on to develop ARF. This disorder is less common in children than adults.

Urine output criteria GFR criteria Increased creatinine х1.5 or GFR decrease >25% UO < 0,5 ml kg -1 h -1 x 6 h Risk Injury Increased creatinine ×2 or GFR decrease >50% UO < 0,5 ml kg -1 h -1 x 12 h Increased creatinine x 3 or GFR decrease > 75% or creatinine ≥ 4mg per 100ml (acute rise of ≥ 0,5mg per 100 ml dl) Oliguria Failure UO<0,3 ml kg -1 h-1x 24 h or anuria x 12 h Persistent ARF = complete loss of renal function > 4 weeks Loss End-stage renal disease ESRD

Etiology of acute renal failure three major categories: prerenal - those that decrease renal blood flow intrarenal - those that produce a renal parenchymal insult postrenal or obstructive - those that obstruct urine flow.

Prerenal Causes of Acute Renal Failure

Pathophysiology of Prerenal ARF Results from a decrease in renal blood flow. The glomerular filtration rate (GFR) is reduced and the kidney retains water and salt, causing oliguria, production of a concentrated urine, and a progressive inability to excrete nitrogenous wastes.

Pathophysiology of Intrarenal Acute Renal Failure: a) Glomerular Disease: Most of the glomerular disease producing ARF. Progression of the inflammatory process leads to destruction of glomerulus and a decrease in the GFR. b) ATN: The exact cause of this is not clear. c) Interstitial Disease: An inflammatory process is initiated in the renal interstitium in response to a wide variety of stimuli (toxic, metabolic, infectious, immune, infiltrative), although drugs are probably the most common causes.

Pathophysiology of Postrenal Acute Renal Failure: A simple mechanical or functional obstruction to the free flow of urine precludes its excretion, producing renal failure.

Diagnosis of acute renal failure History and physical exam: Evaluation of the medical history, physical exam findings, and the results of a few radiographic studies is often necessary to determine the cause of acute renal failure Often, the history alone can suggest the cause as being prerenal, renal, or post-renal. Physical exam is usually most helpful in assessing the volume status of a patient.

Examination of the Urine:

The BUN also rises with renal dys- function Serum and Urine Chemical Analysis: changes in the serum creatinine level is a result of a change in the GFR. Abrupt cessation of GF causes the serum creatinine to rise by 1-3 mg/dl daily The BUN also rises with renal dys- function Serum BUN to creatinine ration of greater than 20 suggests prerenal azotemia rather than ATN, which is associated with a level of 10 to 1.

Urine Osmolality: Normally, the kidney can concentrate urine to levels greater than 1,200 mOsm/kg. Serum osmolality levels greater than 500 mOsm/kg suggest prerenal azotemia. In ATN the Urine osmolality is approximately 300-350, which is similar to the serum osmolality.

Urine Sodium Concentration: If the kidney is responding appropriately to a decreased effective intravascular volume, urine sodium concentration will usually be low (less than 20 mEq'L). The fractional excretion of sodium (FENa) This can be calculated as follows: FENa (%) = (Urine sodium / plasma sodium) x 100 (Urine creat. / plasma creat) In prerenal azotemia and acute glomerulonephritis, FENa is less than 1%. If ARF is associated with intrinsic renal disease, urine sodium is usually greater than 40 mEq/L and FENa is greater than 2%

Other Indices: Urine/Serum Creatinine Ratio Urine/Serum Urea Ratio Creatinine clearance Free Water clearance.

RADIOGRAPHIC PROCEDURES Intravenous Pyelogram: IVP provides an anatomic picture of the kidney At this time there is little indication for IVP in the patient with ARF. Ultrasonography: It is a sensitive test for obstruction (93-98%) and provides information about kidney size (the kidney size can be helpful in judging the chronicity of the kidney disease). Computed tomography (CT): Hydronephrosis can be recognized without contrast. The cause of obstruction (Ex. lymphoma, retroperitoneal fibrosis, etc) can often be delineated.

Other Tests: Radionuclide scans can be used if there is a concern about vascular perfusion of the kidneys. Percutaneous nephrostomy combined with antegrade pyeography can be employed to diagnose the precise level of obstruction in the urinary tract. if the diagnosis is still unclear, the patient may need a renal biopsy.

ACUTE TUBULAR NECROSIS tubular necrosis with sloughing of the epithelial cells occlusion of the tubular lumina by casts and by cellular debris backleak of filtrate across the damaged tubular epithelia primary reduction in glomerular filtration resulting both from arteriolar vasoconstriction and from mesangial contraction.

Major Causes of Acute Tubular Necrosis Renal Ischemia: * Severe prerenal disease from any cause. Exposure to Nephrotoxins: * Amphotericin B * Aminoglycosides * Heme Pigments * NSAID's * Radiocontrast agents * Pentamidine * Cisplatin * Acyclovir

COMPLICATIONS of ACUTE RENAL FAILURE Cardiovascular System: CHF, MI, and cardiac arrest Pulmonary System Complications: Pulmonary infiltrates due to edema from volume overload and/or infection Gastrointestinal System Complications: severe nausea, vomiting, and anorexia, upper GI bleeding, stress ulcers and gastritis.

COMPLICATIONS of ACUTE RENAL FAILURE Neurologic System Complications: lethargy, somnolence, lassitude, and fatigue, irritability, confusion, disorientation, decreased memory, twitching, asterixes, and myoclonus. In advanced cases - generalized seizures with somnolence and coma. Infectious Complications: pulmonary, urinary infections and peritonitis. Disorders of Electrolyte Metabolism: Hyperkalemia, hyponatremia, metabolic acidosis, and hyperuricemia

TREATMENT OF ACUTE RENAL FAILURE Postrenal Failure: In those with postrenal failure, a passage for the drainage of urine must be created. The exact method that is used will depend entirely on the level of the obstruction and may be as simple as a urinary catheter ,or as complex as a percutaneous nephrostomy tube

TREATMENT OF ACUTE RENAL FAILURE Prerenal Failure (Remember the etiologies): Treatment for True Volume Depletion: is aimed at restoration of the normal circulating blood volume. Initially fluid boluses may be needed, and if indicated blood transfusion may be required. The adequacy of fluid repletion can be assessed from physical exam and by monitoring renal function and urine output

TREATMENT OF ACUTE RENAL FAILURE Treatment for ARF due to Advanced Liver Disease: Dietary sodium restriction and periods of bed rest Diuretics therapy:the preferred agent is spironolactone. Paracentesis may be helpful in those patients with tense ascities. Albumen may be given at the same time to help prevent the worsening of intravascular depletion. A peritoneovenous shunt, which drains into the internal jugular vein and translocates the ascitic fluid into the vascular space.

TREATMENT OF ACUTE RENAL FAILURE Treatment of ARF Caused by Congestive Heart Failure: The use of diuretics may be of some help as this will increase the renal output. Another option is a trial of iatrogenic agents to help increase cardiac output and thus increase renal perfusion. ACE inhibitors may also be helpful.

TREATMENT OF ACUTE RENAL FAILURE Renal Causes of ARF: identify the cause of the intrinsic renal failure, keeping in mind the multitude of known possible causes. Most commonly, the cause of the intrinsic renal failure will be from ATN. Attention must be paid to maintenance of the fluid and electrolyte balance and to proper nutrition. Despite management, some patients will require dialysis

TREATMENT OF ACUTE RENAL FAILURE The use of diuretics - Lasix in high dose and mannitol. Dopamine may be an effective agent along with furosimide in an effort to increase urine output.

TREATMENT OF ACUTE RENAL FAILURE Indications for dialysis include: * marked fluid overload * severe hyperkalemia * presence of uremic signs or symptoms (pericarditis, confusion, bleeding with coagulopathy present) * severe metabolic acidosis (controversial) * BUN levels greater than 100