Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android

Kidneys may be damaged by a variety of injuries. Data helpful in the evaluation of kidney disease include estimation of disease duration, eGFR, examination of the urine, and quantification of urinary protein excretion. Additionally, renal imaging (most often ultrasonography) can be helpful. Kidney biopsy may be performed in select cases as noted below, particularly when glomerular disease is suspected.


Kidney disease can be acute or chronic. AKI is worsening of kidney function over hours to days, resulting in retention of waste products (such as urea nitrogen) and creatinine in the blood. Retention of these substances is called azotemia. CKD is the loss of kidney function over months to years. Differentiating between AKI and CKD is important for diagnosis and treatment, and certain clues may help distinguish the two. For instance, oliguria is only observed in AKI, whereas anemia (from low kidney erythropoietin production) suggests CKD. Additionally, small kidney size on imaging is more consistent with CKD, whereas normal to large kidney size can be seen with both AKI and CKD.


Examination of the urine can provide important clues when evaluating kidney disease. A urine specimen should be collected midstream or by bladder catheterization and examined within 1 hour after collection to avoid destruction of formed elements. UA includes dipstick examination followed by microscopy if the dipstick has positive findings. The dipstick examination measures urinary pH, specific gravity, protein, hemoglobin, glucose, ketones, bilirubin, nitrites, and leukocyte esterase. Microscopy of centrifuged urinary sediment permits examination of formed elements—crystals, cells, casts, and infectious organisms. A bland (normal) sediment is common, especially in CKD and acute nonparenchymal disorders, such as limited effective blood flow to the kidney or urinary obstruction. Urinary casts form when urine flow is slow, leading to precipitation of Tamm-Horsfall mucoprotein in the renal tubule; if there are many red or white blood cells in the urine, cellular casts may form. The presence of protein on dipstick examination suggests underlying glomerular disease. If the glomerular basement membrane (GBM) is damaged (eg, by inflammation), RBCs may leak into the urinary space and appear dysmorphic. Thus, proteinuria, dysmorphic hematuria, and RBCs casts (eFigure 22–1) are highly suggestive of glomerulonephritis. If proteinuria is significant, it is classified as nephrotic-range; significant proteinuria accompanied by lipiduria may indicate nephrotic syndrome. Granular casts (also called “muddy brown casts”) and renal tubular epithelial cells alone or in casts are hallmarks of ATN. WBCs (including neutrophils and eosinophils), WBC casts (Table 22–1), and proteinuria of varying degree can be seen with pyelonephritis and interstitial nephritis; pyuria alone can indicate UTI.

Table 22–1.Significance of specific urinary casts.

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.