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Overview of the management of chronic kidney disease in adults

Mark Rosenberg, MD
Section Editor
Gary C Curhan, MD, ScD
Deputy Editor
Alice M Sheridan, MD


All patients with renal disease (whether acute or chronic) should undergo an assessment of renal function by estimating the glomerular filtration rate (GFR) from the serum creatinine. This measurement is used clinically to evaluate the degree of renal impairment, to follow the course of the disease, and to assess the response to therapy. An attempt must also be made to obtain a specific diagnosis. The first step in this process is a careful urinalysis, looking for proteinuria, hematuria, and cellular casts. Further evaluation may include quantification of proteinuria, kidney ultrasound, referral to a nephrologist, and a kidney biopsy. Nephrology referral is especially indicated when there is a rapid decline in kidney function, an elevated albumin-to-creatinine ratio (>300 mg/g), or urinary red blood cell casts. (See "Assessment of kidney function" and "Diagnostic approach to adult patients with subacute kidney injury in an outpatient setting" and "Urinalysis in the diagnosis of kidney disease".)

An overview of the general issues involved in the management of the patient with chronic kidney disease (CKD), including modalities to slow the rate of progression, will be presented here. The specific therapy of patients with particular renal diseases is discussed separately in the appropriate topic reviews.


The initial injury to the kidney may result in a variety of clinical manifestations, ranging from asymptomatic hematuria to renal failure requiring dialysis. Many individuals fully recover and subsequently suffer from little or no sequelae. Poststreptococcal glomerulonephritis in children, for example, most frequently has a long-term benign prognosis. By comparison, some patients, such as those with lupus nephritis, experience repeated and chronic insults to the kidney, thereby resulting in lasting damage. Furthermore, others in whom the initial disease is either inactive or cured may still develop progressive renal disease due to hemodynamic and other mechanisms.

In addition to variations in the activity of the individual diseases, these different manifestations are partly due to how the kidney responds to injury. The kidney is able to adapt to damage by increasing the filtration rate in the remaining normal nephrons, a process called adaptive hyperfiltration. As a result, the patient with mild renal insufficiency often has a normal or near-normal serum creatinine concentration. Additional homeostatic mechanisms (most frequently occurring within the renal tubules) permit the serum concentrations of sodium, potassium, calcium, and phosphorous and the total body water to also remain within the normal range, particularly among those with mild to moderate renal failure. (See "Assessment of kidney function".)

Adaptive hyperfiltration, although initially beneficial, appears to result in long-term damage to the glomeruli of the remaining nephrons, which is manifest by proteinuria and progressive renal failure. This process appears to be responsible for the development of renal failure among those in whom the original illness is either inactive or cured [1]. Estimates of single nephron glomerular filtration rate (GFR) (SNGFR) in humans support hyperfiltration as a relevant pathophysiologic mechanism [2]. An elevated SNGFR was associated with risk factors for progression including obesity, a family history of end-stage renal disease (ESRD), and more glomerulosclerosis and arteriosclerosis suggesting compensation in remaining nephrons to maintain total GFR. The institution of measures to help prevent this process, such as antihypertensive therapy with an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB), may slow progressive disease and even preserve renal function. If these modalities are effective, the benefit is likely to be greatest if begun before a great deal of irreversible scarring has occurred. (See "Secondary factors and progression of chronic kidney disease".)

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Literature review current through: Sep 2017. | This topic last updated: Sep 25, 2017.
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