ABSTRACT: Certain indicators derived from noninvasive testing can categorize kidney diseases into clinically relevant groups. The results of select tests— estimates of glomerular filtration rate (GFR), renal ultrasound scans, and urinalysis, in conjunction with urinary protein measurements—can be used to determine whether renal injury is acute or chronic, glomerular or interstitial, in a systematic manner. First, GFR can be estimated and kidney disease staged if it is chronic (of greater than 3 months’ duration). Then, ultrasound examination can further determine the duration of disease, the presence of obstruction, and the possibility of a solitary functioning kidney or other anatomic abnormalities. Finally, urinalysis and spot urine evaluations for both protein and creatinine can lead to determinations that implicate the glomerulus or interstitium as the origin of renal injury.
Key words: chronic kidney disease, renal disease
Chronic kidney disease (CKD) has become a burgeoning epidemic. Patients with various stages of CKD initially seek care from their primary care physician; some of these patients sustain acute, reversible renal injuries as well.
If the renal injury is to be reversed, or at least slowed in its progression to dialysis dependence, its presence and cause must be ascertained. Timely nephrology referral and appropriate treatment—such as blood pressure control with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)—have become commonplace management tools in primary care practice.
In this article, we present a diagnostic algorithm designed to streamline the approach to kidney disease for primary care practitioners. The Algorithm relies on select noninvasive tests—estimates of glomerular filtration rate (GFR), renal ultrasound scans, and urinalysis, in conjunction with urinary protein measurements—to categorize disease processes and to determine whether renal injury is acute or chronic, glomerular or interstitial, in a systematic manner. Despite its simplicity, this approach is accurate, inexpensive, and efficient. We will also apply the algorithm to real-world cases representative of those seen in primary care practice.
NOMENCLATURE AND ETIOLOGY OF RENAL DISEASE: SOURCES OF CONFUSION
The complex vocabulary surrounding kidney disease has been in constant flux and, as a result, multiple names have been used for the same disease. Thus, it should come as no surprise that unnecessary confusion has been engendered. For example, during the past generation, minimal-change disease, lipoid nephrosis, and nil disease have been used interchangeably to describe the same nephrotic lesion. Another example is rapidly progressive glomerulonephritis (RPGN) and crescentic glomerulonephritis. Both names describe the same pathology comprising glomerular crescents on renal biopsy and a rapidly progressive decline in renal function.
To further complicate the issue, the etiology of RPGN has exploded into a confusing laundry list of diseases that run the gamut from Wegener granulomatosis to Henoch-Schönlein purpura. If competing names are not enough, some diseases, such as diabetic renal failure, can lead to a chronic vascular renal injury (nephrosclerosis) without significant proteinuria, a glomerular injury with nephrotic range proteinuria, or even acute kidney failure as a consequence of contrast media administration.
The confusion has caused some physicians to avoid renal diagnostic evaluations completely. Now that kidney disease has become a common problem—presenting to primary care at a stage at which it is still treatable—this avoidance has become unacceptable. If a decline in the number of persons who progress to dialysis dependence is to be realized, or at least a slowing of progression, primary care has to become the critical diagnostic and therapeutic interface for kidney disease.
PRIMARY CARE: THE FRONT LINE IN MANAGING RENAL DISEASE
Typically, physicians are confronted with evidence of kidney disease through abnormal urinalysis results or an elevated serum creatinine level, frequently in patients for whom past information is meager. The abnormality is often “quantitated” either in terms of a decreased GFR or “dipstick 1-4+” proteinuria.
The initial steps in diagnosis are critical: to establish through imaging whether deficits in kidney function, or GFR, are acute or chronic. The latter is defined as decreased GFR or structural kidney damage of greater than 3 months’ duration. Then, judiciously chosen tests guide a diagnostic scheme that when followed systematically implicates the site of renal injury through a reliance on measurement of urinary protein and sediment (see Algorithm). As Cases 1 through 4 will illustrate, a structural examination of the kidneys with ultrasonography, paired with a noninvasive “biopsy” of the urine through urinalysis, serves as an effective primary care entry into the diagnostic process.
Ultrasonography remains the screening test of choice for pinpointing urinary tract obstruction as well as differentiating acute from chronic renal disease on the basis of kidney size. Additional information obtained from the ultrasound, such as the discovery of cysts in patients with autosomal dominant polycystic kidney disease (ADPKD) or the detection of a renal size disparity suggestive of renal artery stenosis, is provided without further cost or administration of contrast.
The urinalysis forms the basis both for identifying patients with glomerular disease and for broadly categorizing such diseases as either “nephritic” or “nephrotic.” Since only primary care is designed to span multiple organ systems simultaneously, the diagnosis of serious systemic diseases with renal manifestations—for instance kidney, electrolyte (calcium), bone, and blood abnormalities accompanying multiple myeloma—can be quickly “pieced together” through the renal algorithm.
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The authors report that they have no relevant financial relationships to disclose.