In this chapter, the pathology of the kidney is organized into four anatomic categories: diseases of the glomeruli, tubules, interstitium, and vessels. Diseases that affect the glomeruli often have an immunologic etiology, whereas those that affect the tubules and interstitium usually have an infectious or toxic etiology. Early in the disease process, most disorders predominantly affect one of the anatomic structures listed above. Over time, however, the entire kidney usually becomes diseased. Because of the large physiologic reserve of the kidneys, many diseases do not become clinically apparent until the majority of the organ is affected, making subtle abnormalities in laboratory findings the only early indication of renal disease. Recognition of these patterns of abnormalities, pathologic findings, and clinical presentation is perhaps more important to renal pathology than in any other organ system. This chapter describes acute and chronic renal failure, disorders of volume regulation, glomerular diseases, tubulointerstitial diseases, nephrolithiasis, cystic diseases of the kidney, renal tumors, pathology of the bladder, acid-base disorders, and electrolyte disorders.
Overview: Acute renal failure is rapid onset of azotemia (i.e., elevated blood urea nitrogen [BUN] and creatinine [Cr]) combined with oliguria or anuria. Azotemia can occur by itself, in which case a patient has an elevated BUN and creatinine but normal urine output. Therefore, the difference between azotemia and acute renal failure is the amount of urine output (normal with azotemia; decreased or absent with acute renal failure). There are three types of acute renal failure and azotemia: prerenal, intrinsic (i.e., renal), and postrenal, which are based upon the location of the source of the azotemia or acute renal failure. To simplify the following discussion, the three forms will be listed as prerenal azotemia, intrinsic azotemia, and postrenal azotemia; however, remember that azotemia and acute renal failure are technically on a spectrum defined by urine output. For example, the listed causes of prerenal azotemia can also lead to acute renal failure.
Basic description: Source of azotemia originates proximal to the kidney.
Causes: Low-volume stimulus caused by hypovolemia, heart failure, sepsis, and renal vascular pathology (e.g., atherosclerosis, fibromuscular dysplasia).
Important point regarding prerenal azotemia: In prerenal azotemia, the kidney functions normally and responds to a perceived low-volume stimulus by reabsorption of sodium (FENa < 1%), water, and urea. Because creatinine is filtered and secreted by the tubules, and urea is filtered and reabsorbed, the low-volume stimulus in prerenal azotemia causes a rise in serum BUN out of proportion to the rise in serum creatinine. Therefore, in the absence of other causes of alterations in BUN and creatinine (e.g., gastrointestinal bleed, rhabdomyolysis), the BUN/Cr ratio is usually > 20.
Basic description: Source of azotemia originates within the kidney.
Causes: Acute tubular necrosis (toxic or ischemic type), glomerular disease, acute interstitial nephritis.
Important point: Intrinsic azotemia implies dysfunction of the kidney itself. In the setting of a normal kidney, oliguria would be expected to be accompanied by avid sodium retention. Intrinsic azotemia, however, is characterized by FENa > 1% due to impaired tubular function. The BUN/Cr ratio is < 20 because of normal hemodynamics.
Basic description: Azotemia due to obstruction of the urinary tract. The source of renal failure originates distal to ...