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Kunjan Shah Internal Medicine Dr.

Hussain Acute Kidney Failure Patients with kidney disease may have a variety of different clinical presentations. Some have symptoms or signs that are directly referable to the kidney (hematuria, flank pain) or to associated extrarenal manifestations (edema, hypertension, signs of uremia), but many patients are asymptomatic and are noted on routine examination to have an elevated serum creatinine concentration or an abnormal urinalysis (such as microscopic hematuria or proteinuria). GFR must first be estimated by measurement of the serum creatinine concentration. Careful xamination of the urine also help narrow the findings. The causes of acute kidney injury are isolated to specific areas of the kidney or surrounding structures. Blood from the renal arteries is delivered to the glomeruli. The glomeruli form an ultrafiltrate of plasma that is free of protein and blood elements, which flows into the renal tubules. The tubules reabsorb and/or secrete solutes and reabsorb almost all of the filtered water. The final tubular fluid, urine, leaves the kidney and drains into the renal pelvis, ureter, bladder and excreted thru urethra. Prerenal causes include those that decrease effective blood flow to kidney, such as low blood volume, low BP, and heart failure. Renal artery stenosis is also a cause, which is a narrowing of the renal artery and renal vein thrombosis which is a clot that forms in the renal vein. These causes inadequate cardiac output and hypovolemia which reduces perfusion of both kidneys. Intrinsic causes are sources of damage to the kidneys. This can be due to damage to the glomeruli, renal tubules, or interstitium. Common causes include glomerulonephritis, ATN, and AIN. Postrenal causes are typically due to an obstruction such as in BPH, kidney stones, obstructed urinary catheter, bladder stone, bladder/ureteral/renal malignancy. It is useful to perform a bladder scan or post void residual to rule out urinary retention. Patients with AKI or CKD can present with signs and symptoms resulting directly from diminished kidney function, including edema, hypertension, flank pain, and decreased urine output. Symptoms and signs of renal failure include weakness and easy fatigability, anorexia, vomiting, mental status changes, and seizures. Lab findings that are suggestive include an elevation in serum creatinine, hyperkalemia, and on UA albuminuria, or abnormal urine sediment. Systemic symptoms including fever, arthralgias, pulmonary lesions are suggestive of systemic disease, such as vasculitis or lupus. Unilateral flank pain is consistent with obstruction, infarction or infection. As examples, edema, hypertension, hematuria with red cell casts, and a rapidly rising serum creatinine concentration is almost certainly due to acute glomerulonephritis or renal vasculitis, while edema, heavy proteinuria, and little or no hematuria is indicative of a nonproliferative glomerular disease such as diabetic nephropathy, membranous nephropathy, or minimal change disease. An important aspect of the evaluation of the patient with kidney disease is the determination of disease duration. Acute refers to a rise in serum creatinine concentration or abnormal UA that has developed within hours to days. The criteria for acute kidney

injury include an increase in serum creatinine by 0.3 mg/dL (27 micromol/L) or 1.5 times the baseline value within 48 hours (AKIN criteria), or an increase 1.5 times the baseline value within seven days. Rapidly progressive is kidney disease that progresses for weeks. Chronic is a glomerular filtration rate less than 60 mL/min per 1.73 m2 for three months or more and/or evidence of kidney damage such as albuminuria, urine sediment abnormalities, or findings on renal imaging or renal biopsy. Estimation of the glomerular filtration rate (GFR) gives an approximate measure of the number of functioning nephrons. A reduction in GFR implies either progression of the underlying disease or the development of a superimposed and often reversible problem, such as decreased renal perfusion due to volume depletion. An increase in GFR, on the other hand, is indicative of improvement in kidney function, whereas a stable GFR implies stable disease. The FENa is the most accurate screening test to differentiate between prerenal disease and ATN. A value below 1 percent suggests prerenal disease, where the reabsorption of almost all of the filtered sodium represents an appropriate response to decreased renal perfusion. In comparison, while a value above 2 percent usually indicates ATN, while a value between 1 and 2 percent can be seen with either disorder. Because of safety, ease of use, and the information provided, the most commonly used radiographic technique in patients presenting with renal disease is renal ultrasonography. Since obstruction is a readily reversible disorder, all patients presenting with acute or chronic renal failure of unknown etiology should undergo ultrasonography, the modality of choice to assess possible obstructive disease. A renal biopsy is most commonly obtained in patients with suspected glomerulonephritis or vasculitis and in those with otherwise unexplained acute or subacute renal failure. Volume status should be assessed in all patients with AKI. Fluid should be given to restore intravascular volume in patients who are volume depleted. The amount of administered fluid and the rate of replacement should be targeted to defined endpoints such as mean arterial pressure. Types of replacement fluid include colloid- and crystalloid solutions-containing solutions. For patients with AKI who require replacement fluid, we generally use non-potassium-containing crystalloid solution such as normal saline rather than colloid-containing solutions. Diuretics should not be used for prolonged therapy in place of dialysis. Diuretics may be used for a limited period of time to relieve signs and symptoms of volume overload Loop diuretics may be more effective than thiazides at glomerular filtration rate less than 30 mL/min per 1.73m2. Metabolic acidosis is common among patients with AKI. In general we dialyze patients with AKI who are volume overloaded and have a pH<7.1 meq/L. Dialysis is preferred to the administration of bicarbonate among such patients because bicarbonate administration results in a large sodium load that may cause or contribute to volume overload. Among patients with AKI who are not volume overloaded and have no other indication for acute dialysis, bicarbonate may be used in the setting of a non-anion gap acidosis related to diarrhea, or in patients with a severe organic acidosis while awaiting dialysis. We do not use bicarbonate therapy in patients with a less severe organic acidosis (pH 7.1 or greater).