Approach to Acute Kidney Disorders

DIAGNOSTIC APPROACH TO ACUTE RENAL FAILURE

APPROACH TO ACUTE KIDNEY DISORDERSBy: Amr Mohammed Abdullah11110053Internal Medicine: NephrologyThe diagnostic approach to AKI involves :Determine of the cause to prerenal, renal, or postrenal categories + refinement of the diagnosis based on additional laboratory testing.History and Physical Examination in Acute Renal FailureAny decrease in effective perfusion of the kidneys can result in the syndrome of prerenal AKI. This may be the result of: absolute decrease in the (ECF) volume, redistribution of ECF from vascular to interstitial locations (third-spacing), suspected in the presence of severe burns, pancreatitis, peritonitis, or recent abdominal surgery.most common in gastrointestinal fluid losses or in patients receiving excessive doses of diuretics.impaired delivery of blood to the kidneys, can occur in patients with renal arterial stenosis, vasculitis, or depressed cardiac function. History and Physical Examination in Acute Renal FailureThe cardinal signs of ECF volume depletion are changes in:hemodynamic parameters.An orthostatic increase in pulse of 15 beats per minute or a decrease in diastolic blood pressure of 10 mm Hg can detect losses of 5% of the ECF volume. A postural increase in pulse (supine to standing) of at least 30 beats per minute is 96% specific for clinically significant volume depletionThe inability of a patient to stand because of severe lightheadedness is a relatively specific sign of hypovolemia. jugular venous pressure.skin.cool, mottled extremities, dry mucous membranes and axillae, and skin tenting (particularly over the forehead and sternum, where age-related changes in skin elasticity are not as pronounced as elsewhere). not particularly sensitive or specific.History and Physical Examination in Acute Renal FailureDecreases in weight, if known, can provide some information about the degree of ECF loss. The importance of changes in weight should be assessed relative to changes in serum sodium concentration. (to know the nature of fluid loss)Effect of fluid loss on body water distribution. Because water is in osmotic equilibrium across biologic membranes, loss of 3 L of solute-free water will be spread across the total body water, resulting in a small decrease (0.3 L) in plasma volume. A similar loss of isotonic fluid, which does not obligate osmotic water movement, leads to a much greater decrease (1.0 L) in plasma volume.

History and Physical Examination in Acute Renal FailureObstruction of the urinary tract must be considered in every patient with an acute deterioration of renal function. Symptoms of acute urinary tract obstruction: (severe flank pain, hematuria, changes in urine flow) often mistaken for urinary tract infection. Identification of preexisting conditions that predispose to urinary tract obstruction is important. History and Physical Examination in Acute Renal FailurePhysical findings suggestive of obstruction include: palpably enlarged kidneys, pelvic or abdominal masses, bladder enlargement, prostatic hypertrophy, aneurysmal dilation of the aorta, and signs of inflammatory bowel disease. If oliguria or anuria develops in a critically ill patient with a Foley catheter in place, possible catheter occlusion should be assessed by:sterile flushing and if necessary a catheter change.Causes of Acute Renal FailurePrerenalVolume depletion: Gastrointestinal fluid loss or hemorrhage; renal losses (diuretics or glucosuria, salt-wasting nephropathy, diabetes insipidus, or adrenal insufficiency); cutaneous losses (burns, desquamation)Volume redistribution: Peripheral vasodilation (sepsis or antihypertensives), peritonitis, burns, pancreatitis, hypoalbuminemia (nephrotic syndrome or hepatic disease)Cardiac dysfunction: Pericardial tamponade, complications of myocardial infarction, acute or chronic valvular disease, cardiomyopathies, arrhythmiasVasodilatory shock: Sepsis, liver failure, postcardiotomy, anaphylaxis, or antihypertensivesRenal vasoconstriction: Cirrhosis, sepsis, hypercalcemia, drugs (cyclosporine, tacrolimus, nonsteroidal anti-inflammatory drugs, or pressors)Causes of Acute Renal FailureRenalIschemia: Trauma, surgery, sepsis, pigment nephropathy (hemolysis or rhabdomyolysis), cardiac or aortic hemorrhageNephrotoxic: Radiocontrast, antibiotics (aminoglycosides or amphotericin), nonsteroidal anti- inflammatory drugs, carbon tetrachloride, ethylene glycol, heavy metals (lead, mercury, arsenic, cadmium, or uranium), pesticides, fungicides, cyclosporine, or tacrolimusDisorders of glomeruli and blood vessels: Poststreptococcal glomerulonephritis, infective endocarditis, systemic lupus erythematosus, Goodpasture syndrome, microscopic polyarteritis, Wegener granulomatosis, Henoch-Schounlein purpura, idiopathic rapidly progressive glomerulonephritis, polyarteritis nodosa, malignant hypertension, thrombotic microangiopathies (hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, postpartum renal failure, or antiphospholipid syndrome), renal artery embolism, renal artery dissection, bilateral renal vein thrombosis, or abdominal compartment syndromeAcute interstitial nephritis:Allergic: Semisynthetic penicillin analogues (eg, methicillin, ampicillin, or nafcillin), cephalosporins, rifampin, ciprofloxacin, cotrimoxazole, sulfonamides, thiazides, furosemide, allopurinol, phenytoin, tetracyclines, or warfarinInfectious: Streptococcal, staphylococcal, leptospirosis, infectious mononucleosis, diphtheria, brucellosis,Legionnaire disease, toxoplasmosis, or cytomegalovirusInfiltrative: Sarcoidosis, lymphoma, leukemiaAutoimmune/alloimmune: Systemic lupus erythematosus or renal transplant rejectionCauses of Acute Renal FailurePostrenalMalignancy: Lymphoma, renal adenocarcinoma, bladder ureteral carcinoma, gynecologic cancers, prostate cancer, other pelvic tumors, or metastatic diseaseInflammatory processes: Tuberculosis, inflammatory bowel disease, retroperitoneal abscess or fibrosis, postradiation therapyVascular diseases: Aortic aneurysm, renal artery aneurysmPapillary necrosis: Diabetes mellitus, sickle hemoglobinopathy, analgesic abuse, prostaglandin inhibition, or hepatic cirrhosisIntratubular: Uric acid, calcium phosphate, Bence Jones proteins, methotrexate, acyclovir, sulfonamide antibiotics, or indinavirMiscellaneous: Nephrolithiasis, ureteral ligation, retrograde pyelography with ureteral edema, neurogenic bladder, neuropathic ureteral dysfunction, or obstructed urinary catheterHistory and Physical Examination in Acute Renal FailureIntrinsic AKI can be the final result of many diverse renal insults. AKI due to therapeutic or recreational drugs (eg, cocaine-induced rhabdomyolysis) is so common that a detailed drug history is mandatory.The presence of a skin rash should suggest a systemic vasculitis with renal involvement or acute tubulointerstitial nephritis. History and Physical Examination in Acute Renal FailurePalpable purpura due to leukocytoclastic vasculitis is characteristic of Henoch-Schnlein purpura. One of the pulmonary-renal syndromes should be considered if prominent thoracic complaints accompany AKI. These include: Goodpasture syndrome, granulomatosis with polyangiitis (formerly known as Wegener granulomatosis), microscopic polyarteritis, systemic lupus erythematosus, and Churg-Strauss syndrome.Diagnostic Tests in Acute Renal FailureThe majority of cases of AKI can be diagnosed by history and physical examination, along with routine clinical testing. But in a significant minority the cause remains obscure after initial assessment, and further evaluation is necessary.Diagnostic Tests in Acute Renal FailureDaily urine volume must be measured in all patients with AKI. Bladder catheterization is both diagnostic and therapeutic in patients with obstruction at the level of the bladder neck or urethra. Diagnostic Tests in Acute Renal FailureUrine volume is determined by the requirement to excrete the daily obligate solute load (electrolytes and nitrogenous wastes) in appropriately concentrated urine. Assuming maximal urine concentrating ability (1400 mOsm/kg), the minimum daily urine output required to excrete the average daily solute load is 400 mL, below which positive solute balance and azotemia develop, thus the standard definition of oliguria (3 suggests nephrotic-range proteinuria, which should be confirmed by 24-hour urine collection). Diagnostic Tests in Acute Renal FailureUrinalysis is also useful in patients with AKI. Glycosuria in the absence of hyperglycemia strongly suggests proximal tubular injury with Fanconi syndrome. A positive reaction for blood in the urine is consistent with acute glomerular or tubular injury, urinary tract infection, or nephrolithiasis. If blood is present on dipstick but not microscopically, or if the findings are disproportionate (eg, 4+ blood on dipstick with rare erythrocytes on microscopy), a pigment nephropathy (hemoglobinuria or myoglobinuria) should be considered. Diagnostic Tests in Acute Renal FailureThe urine sediment is usually unremarkable in prerenal and postrenal azotemia, except for occasional hyaline casts. In postrenal AKI due to stones, blood and crystals can be seen. Intrinsic AKI is often associated with a characteristic (or even diagnostic) urine sediment. A careful microscopic examination frequently can distinguish between GN, AIN, ATN, and TIN. Diagnostic Tests in Acute Renal FailureErythrocyte casts, often accompanied by proteinuria and numerous erythrocytes and leukocytes, are pathognomonic of GN. Detection of large numbers of leukocytes, leukocyte casts, and eosinophils in uninfected urine strongly suggests the diagnosis of drug-induced AIN. ATN is suggested by findings including muddy brown granular casts, free renal tubular cells, and tubular cell casts.noteGN: glomerulonephritisAIN: Acute interstitial nephritisATN: Acute tubular necrosisTIN: Acute tubulointerstitial nephritisDiagnostic Tests in Acute Renal FailureSeveral measurements of urine composition have been suggested as ways to differentiate between prerenal azotemia and intrinsic AKI in the oliguric patient.Urine electrolytes are most useful in this regard, especially the fractional excretion of sodium (FENa), calculated as:

Diagnostic Tests in Acute Renal FailureValues of FENa 0.03 (3%) suggest tubular injury. The FENa is less useful in patients who are not oliguric.may be useful in diuretic-treated patients. Although an elevated value may be a result of ATN or the effects of the diuretic, a low level in the face of diuretic therapy strongly suggests volume depletion and prerenal AKI. Some causes of AKI presenting with a low FENa are listed in next slide. A low UNa ( Acute Kidney Injury and SepsisRenal Disease > Alterations of Kidney Structure & Function in DiseaseThank U