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Chronic Kidney Disease

(Chronic Renal Failure; CKD)


Anna Malkina

, MD, University of California, San Francisco

Last full review/revision Feb 2020| Content last modified Feb 2020

Chronic kidney disease (CKD) is long-standing, progressive deterioration of renal function. Symptoms develop slowly and in advanced stages include anorexia, nausea, vomiting, stomatitis, dysgeusia, nocturia, lassitude, fatigue, pruritus, decreased mental acuity, muscle twitches and cramps, water retention, undernutrition, peripheral neuropathies, and seizures. Diagnosis is based on laboratory testing of renal function, sometimes followed by renal biopsy. Treatment is primarily directed at the underlying condition but includes fluid and electrolyte management, blood pressure control, treatment of anemia, various types of dialysis, and kidney transplantation.

Prevalence of CKD (stages 1 through 5) in the US adult general population is estimated at 14.8%. (For more information, see "CKD in the General Population", which is based on data from the National Health and Nutrition Examination Survey [NHANES, 2018] and the Behavioral Risk Factors Surveillance System [BRFSS, 2018].)

Etiology of CKD

Chronic kidney disease may result from any cause of renal dysfunction of sufficient magnitude (see table Major Causes of Chronic Kidney Disease).

The most common causes in the US in order of prevalence are

Metabolic syndrome, in which hypertension and type 2 diabetes are present, is a large and growing cause of renal damage.

Major Causes of Chronic Kidney Disease



Chronic tubulointerstitial nephropathies

See table Causes of Chronic Tubulointerstitial Nephritis

Glomerulopathies (primary)

Focal segmental glomerulosclerosis

Idiopathic crescentic glomerulonephritis

IgA nephropathy

Membranoproliferative glomerulonephritis

Membranous nephropathy

Glomerulopathies associated with systemic disease


Diabetes mellitus

Anti-GBM antibody disease (also known as Goodpasture syndrome)

Granulomatosis with polyangiitis (formerly known as Wegener's granulomatosis)

Hemolytic-uremic syndrome

Mixed cryoglobulinemia

Postinfectious glomerulonephritis

Systemic lupus erythematosus

Hereditary nephropathies

Autosomal dominant interstitial kidney disease (medullary cystic kidney disease)

Hereditary nephritis (Alport syndrome)

Nail-patella syndrome

Polycystic kidney disease


Hypertensive nephrosclerosis

Obstructive uropathy

Benign prostatic hyperplasia

Posterior urethral valves

Retroperitoneal fibrosis

Ureteral obstruction (congenital, calculi, cancer)

Vesicoureteral reflux

Renal macrovascular disease (vasculopathy of renal arteries and veins)

Renal artery stenosis caused by atherosclerosis or fibromuscular dysplasia

Pathophysiology of CKD

Chronic kidney disease (CKD) is initially described as diminished renal reserve or renal insufficiency, which may progress to renal failure (end-stage renal disease). Initially, as renal tissue loses function, there are few noticeable abnormalities because the remaining tissue increases its performance (renal functional adaptation).

Decreased renal function interferes with the kidneys’ ability to maintain fluid and electrolyte homeostasis. The ability to concentrate urine declines early and is followed by decreases in ability to excrete excess phosphate, acid, and potassium. When renal failure is advanced (glomerular filtration rate [GFR] ≤ 15 mL/min/1.73 m2), the ability to effectively dilute or concentrate urine is lost; thus, urine osmolality is usually fixed at about 300 to 320 mOsm/kg, close to that of plasma (275 to 295 mOsm/kg), and urinary volume does not respond readily to variations in water intake.

Creatinine and urea

Plasma concentrations of creatinine and urea (which are highly dependent on glomerular filtration) begin a hyperbolic rise as GFR diminishes. These changes are minimal early on. When the GFR falls below 15 mL/min/1.73 m2 (normal > 90 mL/min/1.73 m2), creatinine and urea levels are high and are usually associated with systemic manifestations (uremia). Urea and creatinine are not major contributors to the uremic symptoms; they are markers for many other substances (some not yet well defined) that cause the symptoms.

Sodium and water

Despite a diminishing GFR, sodium and water balance is well maintained by increased fractional excretion of sodium in urine and a normal response to thirst. Thus, the plasma sodium concentration is typically normal, and hypervolemia is infrequent unless dietary intake of sodium or water is very restricted or excessive. Heart failure can occur due to sodium and water overload, particularly in patients with decreased cardiac reserve.


For substances whose secretion is controlled mainly through distal nephron secretion (eg, potassium), renal adaptation usually maintains plasma levels at normal until renal failure is advanced or dietary potassium intake is excessive. Potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, beta-blockers, nonsteroidal anti-inflammatory drugs, cyclosporine, tacrolimus, trimethoprim/sulfamethoxazole, pentamidine, or angiotensin II receptor blockers may raise plasma potassium levels in patients with less advanced renal failure.

Calcium and phosphate

Abnormalities of calcium, phosphate, parathyroid hormone (PTH), and vitamin D metabolism can occur, as can renal osteodystrophy. Decreased renal production of calcitriol (1,25(OH)2D, the active vitamin D hormone) contributes to hypocalcemia. Decreased renal excretion of phosphate results in hyperphosphatemia. Secondary hyperparathyroidism is common and can develop in renal failure before abnormalities in calcium or phosphate concentrations occur. For this reason, monitoring PTH in patients with moderate CKD, even before hyperphosphatemia occurs, has been recommended.

Renal osteodystrophy (abnormal bone mineralization resulting from hyperparathyroidism, calcitriol deficiency, elevated serum phosphate, or low or normal serum calcium) usually takes the form of increased bone turnover due to hyperparathyroid bone disease (osteitis fibrosa) but can also involve decreased bone turnover due to adynamic bone disease (with increased parathyroid suppression) or osteomalacia. Calcitriol deficiency may cause osteopenia or osteomalacia.

pH and bicarbonate

Moderate metabolic acidosis (plasma bicarbonate content 15 to 20 mmol/L) is characteristic. Acidosis causes muscle wasting due to protein catabolism, bone loss due to bone buffering of acid, and accelerated progression of kidney disease.


Anemia is characteristic of moderate to advanced CKD (≥ stage 3). The anemia of CKD is normochromic-normocytic, with an Hct of 20 to 30% (35 to 40% in patients with polycystic kidney disease). It is usually caused by deficient erythropoietin production due to a reduction of functional renal mass (see Overview of Decreased Erythropoiesis). Other causes include deficiencies of iron, folate, and vitamin B12.

Symptoms and Signs of CKD

Patients with mildly diminished renal reserve are asymptomatic. Even patients with mild to moderate renal insufficiency may have no symptoms despite elevated blood urea nitrogen (BUN) and creatinine. Nocturia is often noted, principally due to failure to concentrate the urine. Lassitude, fatigue, anorexia, and decreased mental acuity often are the earliest manifestations of uremia.

With more severe renal disease (eg, estimated glomerular filtration rate [eGFR] < 15 mL/min/1.73 m2), neuromuscular symptoms may be present, including coarse muscular twitches, peripheral sensory and motor neuropathies, muscle cramps, hyperreflexia, restless legs syndrome, and seizures (usually the result of hypertensive or metabolic encephalopathy).

Anorexia, nausea, vomiting, weight loss, stomatitis, and an unpleasant taste in the mouth are almost uniformly present. The skin may be yellow-brown. Occasionally, urea from sweat crystallizes on the skin (uremic frost). Pruritus may be especially uncomfortable. Undernutrition leading to generalized tissue wasting is a prominent feature of chronic uremia.

In advanced CKD, pericarditis and gastrointestinal ulceration and bleeding may occur. Hypertension is present in > 80% of patients with advanced CKD and is usually related to hypervolemia. Heart failure caused by hypertension or coronary artery disease and renal retention of sodium and water may lead to dependent edema and/or dyspnea.

Diagnosis of CKD

  • Electrolytes, blood urea nitrogen (BUN), creatinine, phosphate, calcium, complete blood count (CBC)
  • Urinalysis (including urinary sediment examination)
  • Quantitative urine protein (24-hour urine protein collection or spot urine protein to creatinine ratio)
  • Ultrasonography
  • Sometimes renal biopsy

Chronic kidney disease (CKD) is usually first suspected when serum creatinine rises. The initial step is to determine whether the renal failure is acute, chronic, or acute superimposed on chronic (ie, an acute disease that further compromises renal function in a patient with CKD—see table Distinguishing Acute Kidney Injury From Chronic Kidney Disease). The cause of renal failure is also determined. Sometimes determining the duration of renal failure helps determine the cause; sometimes it is easier to determine the cause than the duration, and determining the cause helps determine the duration.

Distinguishing Acute Kidney Injury From Chronic Kidney Disease



Decreased kidney function (estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m2) for ≥ 3 months

Most reliable evidence of CKD

Renal sonogram showing small kidneys

Usually CKD

Renal sonogram showing normal or enlarged kidneys

May be AKI or some forms of CKD (diabetic nephropathy, acute hypertensive nephrosclerosis, polycystic kidney disease, myeloma, rapidly progressive glomerulonephritis, infiltrative diseases [eg, lymphoma, leukemia, amyloidosis], obstruction)

Oliguria, daily increases in serum creatinine and BUN

Probably AKI or AKI superimposed on CKD

No anemia

Probably AKI or CKD due to polycystic kidney disease

Severe anemia, hyperphosphatemia, and hypocalcemia

Possibly CKD but may be AKI

Subperiosteal erosions on radiography

Probably CKD

Chronic symptoms or signs (eg, fatigue, nausea, pruritus, nocturia, hypertension)

Usually CKD

AKI = acute kidney injury; CKD = chronic kidney disease; BUN = blood urea nitrogen.

Testing includes urinalysis with examination of the urinary sediment, electrolytes, urea nitrogen, creatinine, phosphate, calcium, and CBC. Sometimes specific serologic tests are needed to determine the cause. Distinguishing acute kidney injury from CKD is most helped by a history of an elevated creatinine level or abnormal urinalysis. Urinalysis findings depend on the nature of the underlying disorder, but broad (> 3 white blood cell diameters wide) or especially waxy (highly refractile) casts often are prominent in advanced renal failure of any cause.

An ultrasound examination of the kidneys is usually helpful in evaluating for obstructive uropathy and in distinguishing acute kidney injury from CKD based on kidney size. Except in certain conditions (see table Major Causes of Chronic Kidney Disease), patients with CKD have small shrunken kidneys (usually < 10 cm in length) with thinned, hyperechoic cortex. Obtaining a precise diagnosis becomes increasingly difficult as renal function reaches values close to those of end-stage renal disease. The definitive diagnostic tool is renal biopsy, but it is not recommended when ultrasonography indicates small, fibrotic kidneys; high procedural risk outweighs low diagnostic yield.

Stages of chronic kidney disease

Staging CKD is a way of quantifying its severity. CKD has been classified into 5 stages.

  • Stage 1: Normal GFR (≥ 90 mL/min/1.73 m2) plus either persistent albuminuria or known structural or hereditary renal disease
  • Stage 2: GFR 60 to 89 mL/min/1.73 m2
  • Stage 3a: 45 to 59 mL/min/1.73 m2
  • Stage 3b: 30 to 44 mL/min/1.73 m2
  • Stage 4: GFR 15 to 29 mL/min/1.73 m2
  • Stage 5: GFR < 15 mL/min/1.73 m2

GFR (in mL/min/1.73 m2) in CKD can be estimated by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) creatinine equation (1): 141 × (serum creatinine) -1.209× 0.993 age. The result is multiplied by 1.018 if the patient is female and by 1.159 if the patient is African American. For female African Americans, the result is multiplied by 1.018 × 1.159 (1.1799). Alternatively, GFR can be estimated using timed (most commonly 24 hours) urine creatinine clearance using measured serum and urine creatinine; this equation tends to overestimate GFR by 10 to 20%. It is used when serum creatinine assessment may not be as accurate (eg, in patients who are sedentary, very obese, or very thin). Serum cystatin C is an alternative endogenous GFR marker used as a confirmatory test in people with nonrenal factors affecting serum creatinine level (eg, extremely high or low muscle mass, exogenous creatine intake, amputations or neuromuscular diseases, and high protein or exclusively plant-based diets). GFR is calculated using CKD-EPI cystatin C equation (2).

The CKD-EPI formula is more accurate than the Modification of Diet in Renal Disease (MDRD) and Cockcroft-Gault formulas, particularly for patients with a GFR near normal values. The CKD-EPI equation yields fewer falsely positive results indicating chronic kidney disease and predicts outcome better than the other formulas.

Diagnosis references

  • 1. Levey AS, Stevens LA, Schmid CH, et al: A new equation to estimate glomerular filtration rate. Ann Intern Med 150(9):604-612, 2009.
  • 2. Stevens LA, Coresh J, Schmid CH, et al: Estimating GFR using serum cystatin C alone and in combination with serum creatinine: A pooled analysis of 3,418 individuals with CKD. Am J Kidney Dis  51(3):395-406, 2008. doi: 10.1053/j.ajkd.2007.11.018.

Prognosis for CKD

Progression of chronic kidney disease (CKD) is predicted in most cases by the degree of proteinuria. Patients with nephrotic-range proteinuria (> 3 g/24 h or urine protein/creatinine ratio > 3) usually have a poorer prognosis and progress to renal failure more rapidly. Progression may occur even if the underlying disorder is not active. In patients with urine protein < 1.5 g/24 h, progression usually occurs more slowly if at all. Hypertension, acidosis, and hyperparathyroidism are associated with more rapid progression as well.

Treatment of CKD

  • Control of underlying disorders
  • Possible restriction of dietary protein, phosphate, and potassium
  • Vitamin D supplements
  • Treatment of anemia
  • Treatment of contributing comorbidities (eg, heart failure, diabetes mellitus, nephrolithiasis, prostatic hypertrophy)
  • Doses of all drugs adjusted as needed
  • Dialysis for severely decreased glomerular filtration rate (GFR) if symptoms and signs not adequately managed by medical interventions
  • Maintaining sodium bicarbonate level in the normal range 23–29 mmol/L

Underlying disorders and contributory factors must be controlled. In particular, controlling hyperglycemia in patients with diabetic nephropathy and controlling hypertension in all patients substantially slows deterioration of GFR.

For hypertension, some guidelines suggest a target BP of < 140/90 mm Hg, the American Heart Association recommends 130/80, and some authors continue to recommend about 110 to 130/ < 80 mm Hg. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) decrease the rate of decline in GFR in patients with most causes of chronic kidney disease (CKD), particularly those with proteinuria. Increasing evidence suggests that, compared with either drug alone, combined use of ACE inhibitors and ARBs increases incidence of complications and does not slow decline in renal function, even though combined use does reduce proteinuria more.

Activity need not be restricted, although fatigue and lassitude usually limit a patient’s capacity for exercise.

Pruritus may respond to dietary phosphate restriction and phosphate binders if serum phosphate is elevated.


Severe protein restriction in renal disease is controversial. However, moderate protein restriction (0.8 g/kg/day) among patients with eGFR < 60 mL/min/1.73 m2 without nephrotic syndrome is safe and easy for most patients to tolerate. Some experts recommend 0.6 g/kg/day for patients with diabetes and for patients without diabetes if GFR is < 25 mL/min/1.73 m2. Many uremic symptoms markedly lessen when protein catabolism and urea generation are reduced. Also, rate of progression of CKD may slow down. Sufficient carbohydrate and fat are given to meet energy requirements and prevent ketosis. Patients for whom < 0.8 g/kg/day has been prescribed should be closely followed by a dietitian.

Because dietary restrictions may reduce necessary vitamin intake, patients should take a multivitamin containing water-soluble vitamins. Administration of vitamin A and E is unnecessary. Vitamins D2 (ergocalciferol) or D3 (cholecalciferol) are not given routinely but are used based on blood levels of vitamin D 25-OH and PTH.

Dyslipidemia should be addressed. Dietary modification may be helpful for hypertriglyceridemia. Statins are effective for hypercholesterolemia. Fibric acid derivatives (clofibrate, gemfibrozil) may increase risk of rhabdomyolysis in patients with CKD, especially if taken with statin drugs, whereas ezetimibe (which reduces cholesterol absorption) appears relatively safe. Correction of hypercholesterolemia is intended to reduce risk of cardiovascular disease, which is increased in patients with CKD (1).

Mineral and bone disorders

Based on updated KDIGO 2017 clinical practice guidelines (1), it is recommended that serum levels of calcium, phosphate, PTH, vitamin D 25-OH, and alkaline phosphatase activity be monitored beginning in CKD stage 3a. Frequency of monitoring depends on severity of CKD, magnitude of above abnormalities, and frequency of therapeutic interventions. Bone biopsy is the most definitive evaluation to determine the type of renal osteodystrophy.

Hyperphosphatemia should be treated with

  • Dietary phosphate restriction
  • Phosphate binders

Phosphate restriction to 0.8 to 1 g/day of dietary intake is typically sufficient to normalize serum phosphate level in patients with eGFR < 60 mL/min/1.73 m2. Additional intestinal phosphate binders (calcium-containing or non–calcium-containing) may be necessary for adequate control of hyperphosphatemia, which has been associated with increased cardiovascular risk. Non–calcium-containing binders are preferred in patients with hypercalcemia, suspected adynamic bone disease, or evidence of vascular calcification on imaging. If calcium-containing binders are prescribed, then the total dietary and medication sources of calcium should not exceed 2000 mg/day in patients with eGFR < 60 mL/min/1.73 m2.

Vitamin D deficiency should be treated with cholecalciferol (vitamin D3) or ergocalciferol (vitamin D2) to target serum Vitamin D 25-OH level approximately 30-50 ng/mL, as long as there is no hyperphosphatemia or hypercalcemia.

The optimal level of PTH in patients with CKD stages 3a to 5 not on dialysis is not known. However, if PTH levels are progressively rising or are markedly elevated (above 9 times the upper limit of normal for the assay), despite treatment of hyperphosphatemia and vitamin D deficiency, then an active vitamin D analog (for example, calcitriol) is recommended. A typical starting dose is calcitriol 0.25 mcg orally 3 times weekly, titrated to maintain PTH between 2 to 9 times the upper limit of normal for the assay. PTH levels are not corrected to normal because doing so risks precipitating adynamic bone disease.

Fluid and electrolytes

Restricted water intake is required only when serum sodium concentration is < 135 mmol/L or there is heart failure or severe edema.

Sodium restriction of < 2 g/day is recommended for CKD patients with eGFR < 60 mL/m/1.73 m2 who have hypertension, volume overload, or proteinuria.

Potassium restriction is individualized based on serum level, eGFR, dietary customs, and use of drugs that increase potassium levels (eg, ACE, ARBs, or potassium-sparing diuretics). Typically, potassium restriction is not needed with eGFR > 30 mL/min/1.73 m2. Treatment of mild to moderate hyperkalemia (5.1 to 6 mmol/L) entails dietary restriction (including avoiding salt substitutes), correction of metabolic acidosis, and use of potassium-lowering diuretics and gastrointestinal cation exchangers. Severe hyperkalemia (> 6 mmol/L) warrants urgent treatment.

Metabolic acidosis should be treated to bring serum bicarbonate to normal (23–29 mmol/L) to help reverse or slow muscle wasting, bone loss, and progression of CKD. Acidosis can be corrected with oral alkali sources such as sodium bicarbonate or an alkaline-ash diet (primarily fruits and vegetables). Sodium bicarbonate 1 to 2 g orally twice a day is given and the amount is increased gradually until bicarbonate concentration is about 23 mmol/L or until evidence of sodium overloading prevents further therapy. If the alkaline-ash diet is used, serum potassium is monitored because fruits and vegetables contain potassium.

Anemia and coagulation disorders

Anemia is a common complication of moderate to advanced CKD (≥ stage 3) and, when < 10g/dL, is treated with erythropoiesis-stimulating agents (ESA), such as recombinant human erythropoietin (eg, epoetin alfa). Due to risk of cardiovascular complications, including stroke, thrombosis, and death, the lowest dose of these agents needed to keep the Hb between 10 and 11 g/dL is used.

Because of increased iron utilization with stimulated erythropoiesis, iron stores must be replaced, often requiring parenteral iron. Iron concentrations, iron-binding capacity, and ferritin concentrations should be followed closely. Target transferrin saturation (TSAT), calculated by dividing serum iron by total iron binding capacity and multiplying by 100%, should be > 20%. Target ferritin in patients not on dialysis is >100 ng/mL. Transfusion should not be done unless anemia is severe (Hb < 8 g/dL) or causes symptoms.

The bleeding tendency in CKD rarely needs treatment. Cryoprecipitate, red blood cell transfusions, desmopressin 0.3 to 0.4 mcg/kg (20 mcg maximum) in 20 mL of isotonic saline IV over 20 to 30 minutes, or conjugated estrogens 2.5 to 5 mg orally once a day help when needed. The effects of these treatments last 12 to 48 hours, except for conjugated estrogens, which may last for several days.

Heart failure

Symptomatic heart failure is treated with

  • Sodium restriction
  • Diuretics
  • Sometimes, dialysis

Loop diuretics such as furosemide usually are effective even when renal function is markedly reduced, although large doses may be needed. If left ventricular function is depressed, ACE inhibitors (or ARBs) and beta-blockers (carvedilol or metoprolol) should be used. Aldosterone receptor antagonists are recommended in patients with advanced stages of heart failure. Digoxin may be added, but the dosage must be reduced based on degree of renal function.

Moderate or severe hypertension should be treated to avoid its deleterious effects on cardiac and renal function. Patients who do not respond to sodium restriction (1.5 g/day), should receive diuretics. Loop diuretics (eg, furosemide 80 to 240 mg orally twice a day) may be combined with thiazide diuretics (eg, chlorthalidone 12.5 to 100 mg orally once a day, hydrochlorothiazide 25 to 100 mg orally in 1 to 2 divided doses a day, metolazone 2.5 to 20 mg orally once a day) if hypertension or edema is not controlled. Even in renal failure, the combination of a thiazide diuretic with a loop diuretic is quite potent and must be used with caution to avoid overdiuresis.

Occasionally, dialysis may be required to control heart failure. If reduction of the ECF volume does not control blood pressure, conventional antihypertensives are added. Azotemia may increase with such treatment and may be necessary for adequate control of heart failure and/or hypertension.


Renal excretion of drugs is often impaired in patients with renal failure. Common drugs that require revised dosing include penicillins, cephalosporins, aminoglycosides, fluoroquinolones, vancomycin, and digoxin. Hemodialysis reduces the serum concentrations of some drugs, which should be supplemented after hemodialysis. It is strongly recommended that physicians consult a reference on drug dosing in renal failure before prescribing drugs to these very vulnerable patients (2-4).

Most experts recommend avoiding NSAIDs in patients with CKD because they may worsen renal function, exacerbate hypertension, and precipitate electrolyte disturbances.

Certain drugs should be avoided entirely in patients with chronic kidney disease with eGFR < 60 mL/min/1.73m2. They include nitrofurantoin and phenazopyridine. The MRI contrast agent gadolinium has been associated with the development of nephrogenic systemic fibrosis in some patients; because risk is particularly high if patients have estimated GFR < 30 mL/min/1.73m2, gadolinium should be avoided whenever possible in these patients.


Dialysis is usually initiated at the onset of either of the following:

  • Uremic symptoms (eg, anorexia, nausea, vomiting, weight loss, pericarditis, pleuritis)
  • Difficulty controlling fluid overload, hyperkalemia, or acidosis with drugs and lifestyle interventions

These problems typically occur when the estimated GFR reaches ≤ 10 mL/min in a patient without diabetes or ≤ 15 mL/min in a patient with diabetes; patients whose estimated GFR values are near these values should be closely monitored so that these signs and symptoms are recognized early. Dialysis is best anticipated so that preparations can be made and urgent insertion of a hemodialysis catheter can be avoided. Such preparations usually begin when the patient is in early to mid stage 4 CKD; preparation allows time for patient education, selection of the type of dialysis, and timely creation of an arteriovenous fistula or placement of a peritoneal dialysis catheter. (For dialysis preparation, see Hemodialysis.)

Pearls & Pitfalls

  • Begin preparation for dialysis, kidney transplantation, or palliative care during early to mid stage 4 CKD to allow adequate time for patient education and selection of treatment modality, along with any associated preparatory procedures.


If a living kidney donor is available, better long-term outcomes occur when a patient receives the transplanted kidney early, even before beginning dialysis. Patients who are transplant candidates but have no living donor should be placed on the waiting list of their regional transplant center early, because wait times may exceed several years in many regions of the US.

Treatment references

  • KDIGO 2017 Clinical Practice Guidelines for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) Kidney International Supplements 7(1):1-59, 2017.
  • CKD & Drug Dosing: Information for Providers
  • Munar MY, Singh HD: Drug dosing adjustments in patients with chronic kidney disease. Am Fam Physician 75:1487-1496, 2007.
  • Matzke GR, Aronoff GR, Atkinson AJ, et al: Drug dosing consideration in patients with acute and chronic kidney disease—a clinical update from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney International 80:1122–1137, 2011. doi:10.1038/ki.2011.322

Key Points

  • Common causes of chronic kidney disease (CKD) in the US are diabetic nephropathy (the most common), hypertensive nephrosclerosis, glomerulopathies, and metabolic syndrome.
  • Effects of CKD can include hypocalcemia, hyperphosphatemia, metabolic acidosis, anemia, secondary hyperparathyroidism, and renal osteodystrophy.
  • Distinguish CKD from acute kidney injury based on history, clinical findings, routine laboratory tests, and ultrasonography.
  • Control underlying disorders (eg, diabetes) and BP levels (usually with an ACE inhibitor or ARB).
  • Give supplemental vitamin D and/or sodium bicarbonate and restrict potassium and phosphate as needed.
  • Treat heart failure, anemia, and other complications.
  • Educate patients with advanced CKD on treatment options (dialysis, kidney transplantation, or palliative care) early, to allow adequate time for planning.
  • Initiate dialysis for patients with severely decreased eGFR when signs and symptoms are inadequately controlled with drugs and lifestyle interventions.

Drugs Mentioned In This Article

Drug Name Select Trade
hydrochlorothiazide MICROZIDE
sodium bicarbonate No US brand name
ergocalciferol DRISDOL
chlorthalidone THALITONE
desmopressin DDAVP, STIMATE
epoetin alfa EPOGEN/PROCRIT
gemfibrozil LOPID
pentamidine NEBUPENT
tacrolimus PROGRAF
carvedilol COREG
furosemide LASIX
calcitriol ROCALTROL
vancomycin VANCOCIN
metolazone ZAROXOLYN
estrogens Estrogens
ezetimibe ZETIA

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