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Chronic Kidney Disease

(Chronic Renal Failure; CKD)

By

Anna Malkina

, MD, University of California, San Francisco

Last full review/revision Sep 2021| Content last modified Oct 2021
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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 14.9%. (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

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

Table
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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 Heart Failure (HF) Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid... read more Heart Failure (HF) can occur due to sodium and water overload, particularly in patients with decreased cardiac reserve.

Potassium

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 Diuretics A number of drug classes are effective for initial and subsequent management of hypertension: Adrenergic modifiers Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers... read more , angiotensin-converting enzyme inhibitors Angiotensin-converting enzyme (ACE) inhibitors A number of drug classes are effective for initial and subsequent management of hypertension: Adrenergic modifiers Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers... read more , beta-blockers Beta-blockers A number of drug classes are effective for initial and subsequent management of hypertension: Adrenergic modifiers Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers... read more , nonsteroidal anti-inflammatory drugs, Nonopioid Analgesics Nonopioid and opioid analgesics are the main drugs used to treat pain. Antidepressants, antiseizure drugs, and other central nervous system (CNS)–active drugs may also be used for chronic or... read more cyclosporine, tacrolimus, trimethoprim/sulfamethoxazole, pentamidine, or angiotensin II receptor blockers Angiotensin II receptor blockers (ARBs) A number of drug classes are effective for initial and subsequent management of hypertension: Adrenergic modifiers Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers... read more 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 Vitamin D Deficiency and Dependency Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more can occur, as can renal osteodystrophy. Decreased renal production of calcitriol (1,25(OH)2D, the active vitamin D hormone) contributes to hypocalcemia Hypocalcemia Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more . Decreased renal excretion of phosphate results in hyperphosphatemia Hyperphosphatemia Hyperphosphatemia is a serum phosphate concentration > 4.5 mg/dL (> 1.46 mmol/L). Causes include chronic kidney disease, hypoparathyroidism, and metabolic or respiratory acidosis. Clinical features... read more . 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 Metabolic Acidosis Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal... read more (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

Anemia is characteristic of moderate to advanced CKD ( stage 3). The anemia of CKD is normochromic-normocytic, with a hematocrit of 20 to 30% (35 to 40% in patients with polycystic kidney disease Autosomal Dominant Polycystic Kidney Disease(ADPKD) Polycystic kidney disease (PKD) is a hereditary disorder of renal cyst formation causing gradual enlargement of both kidneys, sometimes with progression to renal failure. Almost all forms are... read more Autosomal Dominant Polycystic Kidney Disease(ADPKD) ). It is usually caused by deficient erythropoietin production due to a reduction of functional renal mass (see page Anemias Caused by Deficient Erythropoiesis Overview of Decreased Erythropoiesis Anemia, a decrease in the number of red blood cells (RBCs), hemoglobin (Hb) content, or hematocrit (Hct), can result from decreased RBC production (erythropoiesis), increased RBC destruction... read more ). Other causes include deficiencies of iron Iron Deficiency Iron (Fe) is a component of hemoglobin, myoglobin, and many enzymes in the body. Heme iron, contained mainly in animal products, is absorbed much better than nonheme iron (eg, in plants and... read more , folate Folate Deficiency Folate deficiency is common. It may result from inadequate intake, malabsorption, or use of various drugs. Deficiency causes megaloblastic anemia (indistinguishable from that due to vitamin... read more , and vitamin B12 Vitamin B12 Deficiency Dietary vitamin B12 deficiency usually results from inadequate absorption, but deficiency can develop in vegans who do not take vitamin supplements. Deficiency causes megaloblastic anemia, damage... read more .

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.

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.

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 Distinguishing Acute Kidney Injury From Chronic Kidney Disease 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... read more 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.

Table
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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 Acute Kidney Injury (AKI) Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more from CKD Chronic Kidney Disease 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... read more Chronic Kidney Disease 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 Obstructive Uropathy Obstructive uropathy is structural or functional hindrance of normal urine flow, sometimes leading to renal dysfunction (obstructive nephropathy). Symptoms, less likely in chronic obstruction... read more and in distinguishing acute kidney injury from CKD based on kidney size. Except in certain conditions (see table Major Causes of Chronic Kidney Disease Major Causes of Chronic Kidney Disease 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... read more 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 Renal biopsy Biopsy of the urinary tract requires a trained specialist (nephrologist, urologist, or interventional radiologist). Indications for diagnostic biopsy include unexplained nephritic or nephrotic... read more , 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 Diagnosis references 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... read more Diagnosis references ): 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 Diagnosis references 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... read more Diagnosis references ).

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. doi: 10.7326/0003-4819-150-9-200905050-00006

  • 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 Hypertension Hypertension is sustained elevation of resting systolic blood pressure (≥ 130 mm Hg), diastolic blood pressure (≥ 80 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential... read more Hypertension , acidosis Metabolic Acidosis Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal... read more , and hyperparathyroidism Hypocalcemia Hypocalcemia is a total serum calcium concentration 8.8 mg/dL ( 2.20 mmol/L) in the presence of normal plasma protein concentrations or a serum ionized calcium concentration 4.7 mg/dL ( 1.17... read more 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 Proteinuria Proteinuria is protein, usually albumin, in urine. High concentrations of protein cause frothy or sudsy urine. In many renal disorders, proteinuria occurs with other urinary abnormalities (eg... read more more. Sodium-glucose cotransporter-2 (SGLT2) inhibitors delay progression of proteinuric CKD in patients with or without diabetes, although these drugs are contraindicated in patients with type 1 diabetes mellitus (1, 2 Treatment references 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... read more Treatment references ).

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.

Nutrition

Severe protein restriction in renal disease is controversial. However, moderate protein restriction (0.8 g/kg/day) among patients with estimated GFR (eGFR) < 60 mL/min/1.73 m2 without nephrotic syndrome Overview of Nephrotic Syndrome Nephrotic syndrome is urinary excretion of > 3 g of protein/day due to a glomerular disorder plus edema and hypoalbuminemia. It is more common among children and has both primary and secondary... read more 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 Dyslipidemia Dyslipidemia is elevation of plasma cholesterol, triglycerides (TGs), or both, or a low high-density lipoprotein cholesterol level that contributes to the development of atherosclerosis. Causes... read more 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 Rhabdomyolysis Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle tissue. Symptoms and signs include muscle weakness, myalgias, and reddish-brown urine, although this triad is... read more 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 (3 Treatment references 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... read more Treatment references ).

Mineral and bone disorders

Based on updated KDIGO 2017 clinical practice guidelines (3 Treatment references 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... read more Treatment references ), 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.

  • 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 Hypercalcemia Hypercalcemia is a total serum calcium concentration > 10.4 mg/dL (> 2.60 mmol/L) or ionized serum calcium > 5.2 mg/dL (> 1.30 mmol/L). Principal causes include hyperparathyroidism, vitamin... read more , 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 Vitamin D Deficiency and Dependency Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more 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 Overview of Renal Replacement Therapy Renal replacement therapy (RRT) replaces nonendocrine kidney function in patients with renal failure and is occasionally used for some forms of poisoning. Techniques include continuous hemofiltration... read more 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.

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 Hyperkalemia Hyperkalemia is a serum potassium concentration > 5.5 mEq/L (> 5.5 mmol/L), usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There are... read more (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 Moderate to severe hyperkalemia Hyperkalemia is a serum potassium concentration > 5.5 mEq/L (> 5.5 mmol/L), usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There are... read more (> 6 mmol/L) warrants urgent treatment Emergency treatment Acute kidney injury is a rapid decrease in renal function over days to weeks, causing an accumulation of nitrogenous products in the blood (azotemia) with or without reduction in amount of urine... read more .

Metabolic acidosis Metabolic Acidosis Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal... read more 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

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

Moderate or severe hypertension Hypertension Hypertension is sustained elevation of resting systolic blood pressure (≥ 130 mm Hg), diastolic blood pressure (≥ 80 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential... read more 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 volume of extracellular fluid 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.

Drugs

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 Hemodialysis In hemodialysis, a patient’s blood is pumped into a dialyzer containing 2 fluid compartments configured as bundles of hollow fiber capillary tubes or as parallel, sandwiched sheets of semipermeable... read more 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 (4, 5, 6 Treatment references 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... read more Treatment references ).

Most experts recommend avoiding NSAIDs (nonsteroidal anti-inflammatory drugs) 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 Contrast reactions Sagittal T1-weighted image of the brain shows normal midline structures. Sagittal proton density–weighted 3-tesla magnetic resonance image of the right knee shows meniscocapsular separation... read more Contrast reactions in patients with estimated GFR < 30 mL/min/1.73m2 in the past. More recently, class II gadolinium agents are considered safer and preferred when gadolinium is indicated for patients with eGFR <30 or on dialysis (7 Treatment references 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... read more Treatment references ).

Dialysis

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 Arteriovenous Fistula An arteriovenous fistula is an abnormal communication between an artery and a vein. An arteriovenous fistula may be congenital (usually affecting smaller vessels) or acquired as a result of... read more or placement of a peritoneal dialysis catheter Access Peritoneal dialysis uses the peritoneum as a natural permeable membrane through which water and solutes can equilibrate. Compared to hemodialysis, peritoneal dialysis is Less physiologically... read more . (For dialysis preparation, see Hemodialysis Hemodialysis In hemodialysis, a patient’s blood is pumped into a dialyzer containing 2 fluid compartments configured as bundles of hollow fiber capillary tubes or as parallel, sandwiched sheets of semipermeable... read more .)

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.

Transplantation

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

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).

  • Treat patients with proteinuric CKD with an ACE inhibitor or ARB, plus an SGLT2 inhibitor.

  • 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.

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