100 - Approach to the Patient with Renal Disease

Abstract

The kidneys mediate critical homeostatic functions via excretion of nitrogenous waste and regulated excretion of water, sodium, potassium, calcium, magnesium, phosphate, and acid. The kidney is comprised of about 1 million functional nephrons, and the primary mechanism for excretion is the production of a protein-free and cell-free ultrafiltrate at the vascular origin of the nephron, which is the glomerulus. Renal failure, which refers specifically to a defect in the filtration function, might first be uncovered by abnormalities in blood levels of urea nitrogen, creatinine, and electrolytes. Impaired sodium and water handling in acute kidney injury also may produce symptoms of volume overload, such as edema from decreased urine output. The approach to the patient with renal failure begins by distinguishing acute from chronic processes. Acute renal failure is subdivided into prerenal, intrarenal, and postrenal causes. Prerenal causes include processes that compromise blood flow to the glomerulus. Intrarenal insults (e.g., glomerulonephritis, acute tubular necrosis, and acute interstitial nephritis) affect the kidney’s vasculature, tubules, glomeruli, or interstitium. Postrenal causes can obstruct urine flow at any site within the urinary tract. Acute renal failure usually can be distinguished from chronic renal failure by analyzing the urine for protein, infection, and the presence of abnormal cells, as well as by assessing the trajectory of the serum creatinine level over time. Imaging with ultrasound or computerized tomography may identify the presence of postrenal causes, which commonly result in hydronephrosis. Disorders of water and electrolytes may reflect a defect in renal filtration or tubular function, but they may also be caused by primary gastrointestinal, cardiovascular, or endocrine abnormalities.