Chronic Kidney Disease (CKD)
Updated: Jun 06, 2025
- Author: Pradeep Arora, MD; Chief Editor: Vecihi Batuman, MD, FASN
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Chronic kidney disease (CKD)—or chronic renal failure (CRF), as it was historically termed—is a term that encompasses all degrees of decreased kidney function, from damaged–at risk through mild, moderate, and severe chronic kidney failure. [] CKD is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost.
CKD is more prevalent in the elderly population. Almost half of the patients with CKD are older than 70 years. However, while younger patients with CKD typically experience progressive loss of kidney function, 30% of patients over 65 years of age with CKD have stable disease. []
CKD is associated with an increased risk of cardiovascular disease and end-stage kidney disease (ESKD). Kidney disease is the 9th leading cause of death in the United States. []
The Kidney Disease Outcomes Quality Initiative (KDOQI) of the National Kidney Foundation (NKF) established a definition and classification of CKD in 2002. [] The KDOQI and the international guideline group Kidney Disease: Improving Global Outcomes (KDIGO) subsequently updated these guidelines; the most recent KDIGO update was in 2024. [] These guidelines have allowed better communication among physicians and have facilitated intervention at the different stages of the disease.
The guidelines define CKD as either kidney damage or a decreased glomerular filtration rate (GFR) of less than 60 mL/min/1.73 m2 for at least 3 months. Whatever the underlying etiology, once the loss of nephrons and reduction of functional renal mass reaches a certain point, the remaining nephrons begin a process of irreversible sclerosis that leads to a progressive decline in the GFR. []
Hyperparathyroidism is one of the pathologic manifestations of CKD. See the image below.
See also Chronic Kidney Disease in Children.
A normal kidney contains approximately 1 million nephrons, each of which contributes to the total glomerular filtration rate (GFR). In the face of renal injury (regardless of the etiology), the kidney has an innate ability to maintain GFR, despite progressive destruction of nephrons, as the remaining healthy nephrons manifest hyperfiltration and compensatory hypertrophy. This nephron adaptability allows for continued normal clearance of plasma solutes. Plasma levels of substances such as urea and creatinine start to show measurable increases only after total GFR has decreased 50%.
The plasma creatinine value will approximately double with a 50% reduction in GFR. For example, a rise in plasma creatinine from a baseline value of 0.6 mg/dL to 1.2 mg/dL, although still within the adult reference range, actually represents a loss of 50% of functioning nephron mass.
The hyperfiltration and hypertrophy of residual nephrons, although beneficial for the reasons noted, has been hypothesized to represent a major cause of progressive kidney dysfunction. The increased glomerular capillary pressure may damage the capillaries, leading initially to secondary focal and segmental glomerulosclerosis (FSGS) and eventually to global glomerulosclerosis. This hypothesis is supported by studies of five-sixths nephrectomized rats, which develop lesions identical to those observed in humans with CKD.
Factors other than the underlying disease process and glomerular hypertension that may cause progressive kidney injury include the following:
Thaker et al found a strong association between episodes of acute kidney injury (AKI) and cumulative risk for the development of advanced CKD in patients with diabetes mellitus who experienced AKI in multiple hospitalizations. [] Any AKI versus no AKI was a risk factor for stage 4 CKD, and each additional AKI episode doubled that risk. []
Findings from the Atherosclerosis Risk in Communities (ARIC) Study, a prospective observational cohort, suggest that inflammation and hemostasis are antecedent pathways for CKD. [] This study used data from 1787 cases of CKD that developed between 1987 and 2004.
In children, the GFR increases with age and is calculated with specific equations that are different than those for adults. Adjusted for body surface area, the GFR reaches adult levels by age 2-3 years.
Aspects of pediatric kidney function and the measure of creatinine are informative not only for children but also for adults. For example, it is important to realize that creatinine is derived from muscle and, therefore, that children and smaller individuals have lower creatinine levels independent of the GFR. Consequently, laboratory reports that do not supply appropriate pediatric normal ranges are misleading. The same is true for individuals who have low muscle mass for other reasons, such as malnutrition, cachexia, or amputation.
Another important note for childhood CKD is that physicians caring for children must be aware of normal blood pressure levels by age, sex, and height. Prompt recognition of hypertension at any age is important, because it may be caused by primary renal disease.
Fortunately, CKD during childhood is rare. Pediatric CKD is usually the result of congenital defects, such as posterior urethral valves or dysplastic kidney malformations. Another common cause is FSGS. Genetic kidney diseases also frequently manifest in childhood CKD. Advances in pediatric nephrology have enabled great leaps in survival for pediatric CKD and end-stage kidney disease (ESKD), including for children who need dialysis or transplantation.
The biologic process of aging initiates various structural and functional changes within the kidney. [, ] Renal mass progressively declines with advancing age, and glomerulosclerosis leads to a decrease in renal weight. The number of glomeruli decreases by as much as 30-50% by age 70 years. The GFR peaks during the third decade of life at approximately 120 mL/min/1.73 m2; it then undergoes an annual mean decline of approximately 1 mL/min/1.73 m2, reaching a mean value of 70 mL/min/1.73 m2 at age 70 years.
Ischemic obsolescence of cortical glomeruli is predominant, with relative sparing of the renal medulla. Juxtamedullary glomeruli see a shunting of blood from afferent to efferent arterioles, resulting in redistribution of blood flow favoring the renal medulla. These anatomic and functional changes in renal vasculature appear to contribute to an age-related decrease in renal blood flow.
Renal hemodynamic measurements in aged humans and animals suggest that altered functional response of the renal vasculature may be an underlying factor in diminished renal blood flow and increased filtration noted with progressive renal aging. The vasodilatory response is blunted in the elderly when compared with younger patients.
However, the vasoconstrictor response to intrarenal angiotensin is identical in young and older human subjects. A blunted vasodilatory capacity with appropriate vasoconstrictor response may indicate that the aged kidney is in a state of vasodilatation to compensate for the underlying sclerotic damage.
Given the histologic evidence for nephronal senescence with age, a decline in the GFR is expected. However, the reported rate of GFR decline varies widely because of measurement methods, race, sex, genetic variance, and other risk factors for kidney dysfunction.
Most cases of CKD are acquired rather than inherited, although CKD in a child is more likely to have a genetic or inherited cause. Well-described genetic syndromes associated with CKD include autosomal dominant polycystic kidney disease (ADPKD) and Alport syndrome. Other examples of specific single-gene or few-gene mutations associated with CKD include Dent disease, nephronophthisis, and atypical hemolytic-uremic syndrome (HUS).
APOL1 gene
More recently, researchers have begun to identify genetic contributions to increased risk for development or progression of CKD. Friedman et al found markedly higher rates of hypertension-attributable ESKD and FSGS in individuals who carry two risk alleles of apolipoprotein L1 (APOL1), and these authors estimated that more than 3 million Black persons in the United States may have this high-risk genotype. In contrast, Black individuals without the risk genotype and European Americans appear to have similar risk for developing nondiabetic CKD. []
FGF-23 gene
Circulating levels of the phosphate-regulating hormone fibroblast growth factor 23 (FGF-23) are affected by variants in the FGF23 gene. Isakova et al reported that elevated FGF-23 levels are an independent risk factor for ESKD in patients who have fairly well-preserved kidney function (stages 2-4) and for mortality across the scope of CKD. []
Single-nucleotide polymorphisms
A review of 16 single-nucleotide polymorphisms (SNPs) that had been associated with variation in GFR found that development of albuminuria was associated mostly with an SNP in the SHROOM3 gene. [] Even accounting for this variant, however, there is evidence that some unknown genetic variant influences the development of albuminuria in CKD. This study also suggests a separate genetic influence on development of albuminuria versus reduction in GFR. []
A genome-wide association study (GWAS) that included over 130,000 patients found 6 SNPs associated with reduced GFR. The SNPs are located in or near MPPED2, DDX1, SLC47A1, CDK12, CASP9, and INO80. [] The SNP in SLC47A1 was associated with decreased GFR in nondiabetic individuals, whereas SNPs located in the DNAJC16 and CDK12 genes were associated with decreased GFR in individuals younger than 65 years. []
Immune-system and RAS genes
A number of genes have been associated with the development of ESKD. Many of these genes involve aspects of the immune system (eg, CCR3, IL1RN, IL4). []
Unsurprisingly, polymorphisms in genes involving the renin-angiotensin system (RAS) have also been implicated in predisposition to CKD. One study found that patients with CKD were significantly more likely to have the A2350G polymorphism in the ACE gene, which encodes the angiotensin-converting enzyme (ACE). [] They were also more likely to have the C573T polymorphism in the AGTR1 gene, which encodes the angiotensin II type 1 receptor. []
The ability to maintain potassium excretion at near-normal levels is generally maintained in CKD, as long as aldosterone secretion and distal flow are maintained. Another defense against potassium retention in patients with CKD is increased potassium excretion in the gastrointestinal tract, which also is under control of aldosterone.
Hyperkalemia usually does not develop until the GFR falls to less than 20-25 mL/min/1.73 m2, at which point the kidneys have decreased ability to excrete potassium. Hyperkalemia can be observed sooner in patients who ingest a potassium-rich diet or have low serum aldosterone levels. Common sources of low aldosterone levels are diabetes mellitus and the use of ACE inhibitors, NSAIDs, or beta-blockers.
Hyperkalemia in CKD can be aggravated by an extracellular shift of potassium, such as occurs in the setting of acidemia or from lack of insulin.
Hypokalemia is uncommon but can develop in patients with very poor intake of potassium, gastrointestinal or urinary loss of potassium, or diarrhea or in patients who use diuretics.
Metabolic acidosis may involve a normal anion gap or an increased anion gap; the latter is observed generally with stage 5 CKD but with the anion gap usually not higher than 20 mEq/L. In CKD, the kidneys are unable to produce enough ammonia in the proximal tubules to excrete the endogenous acid into the urine in the form of ammonium. In stage 5 CKD, accumulation of phosphates, sulfates, and other organic anions are the cause of the increase in anion gap.
Metabolic acidosis has been shown to have deleterious effects on protein balance, leading to the following:
Hence, metabolic acidosis is associated with protein-energy malnutrition, loss of lean body mass, and muscle weakness. The mechanism for reducing protein may include effects on adenosine triphosphate (ATP)–dependent ubiquitin proteasomes and increased activity of branched-chain keto acid dehydrogenases.
Metabolic acidosis also leads to an increase in fibrosis and rapid progression of kidney disease, by causing an increase in ammoniagenesis to enhance hydrogen excretion.
In addition, metabolic acidosis is a factor in the development of renal osteodystrophy, because bone acts as a buffer for excess acid, with resultant loss of mineral. Acidosis may interfere with vitamin D metabolism, and patients who are persistently more acidotic are more likely to have osteomalacia or low-turnover bone disease.
Salt and water handling by the kidney is altered in CKD. Extracellular volume expansion and total-body volume overload results from failure of sodium and free-water excretion. This generally becomes clinically manifested when the GFR falls to less than 10-15 mL/min/1.73 m2, when compensatory mechanisms have become exhausted.
As kidney function declines further, sodium retention and extracellular volume expansion lead to peripheral edema and, not uncommonly, pulmonary edema and hypertension. At a higher GFR, excess sodium and water intake could result in a similar picture if the ingested amounts of sodium and water exceed the available potential for compensatory excretion.
Tubulointerstitial renal diseases represent the minority of cases of CKD. However, it is important to note that such diseases often cause fluid loss rather than overload. Thus, despite moderate or severe reductions in GFR, tubulointerstitial renal diseases may manifest first as polyuria and volume depletion, with inability to concentrate the urine. These symptoms may be subtle and require close attention to be recognized. Volume overload occurs only when GFR reduction becomes very severe.
Normochromic normocytic anemia principally develops from decreased renal synthesis of erythropoietin, the hormone responsible for bone marrow stimulation for red blood cell (RBC) production. The anemia starts early in the course of the disease and becomes more severe as viable renal mass shrinks and the GFR progressively decreases.
Using data from the National Health and Nutrition Examination Survey (NHANES), Stauffer and Fan found that anemia was twice as prevalent in people with CKD (15.4%) as in the general population (7.6%). The prevalence of anemia increased with stage of CKD, from 8.4% at stage 1 to 53.4% at stage 5. []
No reticulocyte response occurs. RBC survival is decreased, and bleeding tendency is increased from the uremia-induced platelet dysfunction. Other causes of anemia in CKD include the following:
Renal bone disease is a common complication of CKD. It results in skeletal complications (eg, abnormality of bone turnover, mineralization, linear growth) and extraskeletal complications (eg, vascular or soft-tissue calcification).
Different types of bone disease occur with CKD, as follows:
Bone disease in children is similar but occurs during growth. Therefore, children with CKD are at risk for short stature, bone curvature, and poor mineralization ("renal rickets" is the equivalent term for adult osteomalacia).
CKD–mineral and bone disorder (CKD-MBD) involves biochemical abnormalities related to bone metabolism. CKD-MBD may result from alteration in levels of serum phosphorus, PTH, vitamin D, and alkaline phosphatase.
Secondary hyperparathyroidism develops in CKD because of the following factors:
Calcium and calcitriol are primary feedback inhibitors; hyperphosphatemia is a stimulus to PTH synthesis and secretion.
Hyperphosphatemia and hypocalcemia
Phosphate retention begins in early CKD. When the GFR falls, less phosphate is filtered and excreted, but because of increased PTH secretion, which increases renal excretion, serum levels do not rise initially. As the GFR falls toward CKD stages 4-5, hyperphosphatemia develops from the inability of the kidneys to excrete the excess dietary intake.
Hyperphosphatemia suppresses the renal hydroxylation of inactive 25-hydroxyvitamin D to calcitriol, so serum calcitriol levels are low when the GFR is less than 30 mL/min/1.73 m2. Increased phosphate concentration also affects PTH concentration by its direct effect on the parathyroid glands (posttranscriptional effect).
Hypocalcemia develops primarily from decreased intestinal calcium absorption because of low plasma calcitriol levels. It also possibly results from increased calcium-phosphate binding, caused by elevated serum phosphate levels.
Increased PTH secretion
Low serum calcitriol levels, hypocalcemia, and hyperphosphatemia have all been demonstrated to independently trigger PTH synthesis and secretion. As these stimuli persist in CKD, particularly in the more advanced stages, PTH secretion becomes maladaptive, and the parathyroid glands, which initially hypertrophy, become hyperplastic. The persistently elevated PTH levels exacerbate hyperphosphatemia from bone resorption of phosphate.
Skeletal manifestations
If serum levels of PTH remain elevated, a high ̶ bone turnover lesion, known as osteitis fibrosa, develops. This is one of several bone lesions, which as a group are commonly known as renal osteodystrophy and which develop in severe CKD. Osteitis fibrosa is common in patients with ESKD.
The prevalence of adynamic bone disease in the United States has increased, and its onset before the initiation of dialysis has been reported in some cases. The pathogenesis of adynamic bone disease is not well defined, but possible contributing factors include the following:
Low-turnover osteomalacia in the setting of CKD is associated with aluminum accumulation. It is markedly less common than high-turnover bone disease.
Another form of bone disease is dialysis-related amyloidosis, which has become uncommon since the advent of improved dialysis membranes. This condition occurs from beta-2-microglobulin accumulation in patients who have been on dialysis for at least 8-10 years. It manifests with cysts at the ends of long bones.
Calciphylaxis, or calcific uremic arteriolopathy, results from the deposition of calcium in the arteriolar microvasculature of the deep dermis and subcutaneous adipose tissue. It is is classically associated with CKD, and particularly with ESKD, in patients receiving maintenance dialysis. Although CKD can result in secondary hyperparathyroidism, with increasing serum calcium levels and arteriolar microcalcification, calciphylaxis may develop in individuals with CKD who have normal serum calcium and phosphate concentrations. []
Calciphylaxis typically presents as exquisitely painful retiform purpura or tender nodules, most often on the abdomen and proximal lower extremities, which can progress to cutaneous necrosis. Cutaneous infection may lead to sepsis, which is the most common cause of death in these patients. Reported 1-year mortality rates range from 45% to 80%. []
Causes of chronic kidney disease (CKD) include the following:
Vascular diseases that can cause CKD include the following:
Primary glomerular diseases include the following:
Secondary causes of glomerular disease include the following:
Causes of tubulointerstitial disease include the following:
Urinary tract obstruction may result from any of the following:
In the United States, more than 1 in 7 adults—14% of the adult population, or 35.5 million people—are estimated to have chronic kidney disease (CKD). [] Kidney disease is the ninth leading cause of death in the United States. []
According to the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the overall prevalence of CKD in the US has remained relatively stable since 2004. The largest increase occurred in people with stage 3 CKD, from 4.5% to 6.0%. []
in the US, the prevalence of CKD increases dramatically with age: it is 6% in persons 18 to 44 years, 12% in those 45 to 64 years, and 34% in those 65 or older. [] In the National Health and Nutrition Examination Survey (NHANES) study, the prevalence of stage 3 CKD in individuals younger than 65 years decreased from 1.6% during the years 2013-2016 to 1.3% during the years 2017–March 2020 (the survey was terminated prematurely due to the COVID-19 pandemic), but was virtually unchanged among those age 65 years and older over that period. []
According to 2017–March 2020 NHANES data, the estimated prevalence of CKD in adults by stage was as follows [] :
The adjusted incidence of end-stage kidney disease (ESKD) in the US fell by 8.9% from 20001to 2019. Over that period, however, the number of patients with newly registered ESKD rose from 97,856 to 134,837, an increase of 37.8%. [] In 2023, more than 808,000 people in the US (2 per 1000 population) were currently living with ESKD. []
The US Surgeon General’s latest report on 10-year national objectives for improving the health of all Americans, Healthy People 2030, contains a chapter focused on CKD. For 2030, Healthy People lays out 14 objectives concerning reduction of the US incidence, morbidity, mortality, and health costs of CKD. Reducing kidney failure will require additional public health efforts, including effective preventive strategies and early detection and treatment of CKD.
In 2017, 697.5 million cases of CKD (all stages) were recorded worldwide, for a global prevalence of 9.1%. From 1990 to 2017, the global all-age prevalence of CKD increased 29.3%, whereas the age-standardized prevalence remained stable. Globally, 1.2 million people died from CKD in 2017. The global all-age mortality rate from CKD increased 41.5% from 1990 to 2017. Diabetic nephropathy accounted for almost a third of disability-adjusted life years (DALYs) from CKD. Most of the burden of CKD was concentrated in the three lowest quintiles of the Socio-demographic index (SDI). []
Studies in Europe have reported a range of CKD prevalence, from 3.3% in Norway to 17.3% in Northeast Germany. A study of stages 3-5 CKD using Danish databases found a prevalence of 4.83-4.98% in 2006 to 2013; patients were predominantly women. [] A study using data from 10 major metropolitan areas in China in 2021 reported a CKD crude prevalence of 10.1%. []
In the US, the percentage of adults with CKD is as follows [] :
The prevalence of CKD in Mexican Americans had been lower than in other racial/ethnic groups, but nearly doubled between 2003-2004 and 2015-2016, from 1.6% to 3.5%. [] According to NHANES data, from 2013-2016 to 2017–March 2020, the prevalence of stages 3 and 4 CKD increased in non-Hispanic Blacks, was unchanged in non-Hispanic Whites, and decreased slightly in Hispanics; in contrast, the prevalence of stage 5 CKD decreased in non-Hispanic Blacks but increased slightly in Hispanics. []
The incidence rate of ESKD among Blacks in the United States is nearly 4 times that for Whites. [] Choi et al found that rates of ESKD among Black patients exceeded those among White patients at all levels of baseline estimated glomerular filtration rate (GFR). [] Risk of ESKD among Black patients was highest at an estimated GFR of 45-59 mL/min/1.73 m2, as was the risk of mortality.However, a study by Hicks et al in a large sample of Black patients found that sickle cell trait was not associated with increased risk of diabetic or nondiabetic ESKD. [] Schold et al found that among Black kidney transplant recipients, rates of graft loss and acute rejection were higher than in White recipients, especially among younger patients. []
Important differences also exist in the frequency of specific causes of CKD among different races. In the Chronic Kidney Disease in Children (CKiD) Study, for example, glomerular disease was much more common among nonwhite persons. [] Overall, FSGS in particular is more common among Hispanic Americans and Black persons, as is the risk of nephropathy with diabetes or with hypertension; in contrast, IgA nephropathy is rare in Black individuals and more common among those with Asian ancestry. []
CKD stages 1-4 is slightly more common in women than men, at 14% versus 12%, respectively. [] However, the United States Renal Data System (USRDS) 2023 Annual Data Report notes that for all races in 2021, the adjusted incidence of ESKD was 60.6% higher in men than in women, at 461 cases per million population in males and 287 cases per million population in females. []
CKD in children is somewhat more common in boys, because posterior urethral valves, the most common birth defect leading to CKD, occur only in boys. Importantly, many individuals with congenital kidney disease such as dysplasia or hypoplasia do not clinically manifest CKD or ESKD until adulthood.
Patients with chronic kidney disease (CKD) generally experience progressive loss of kidney function and are at risk for end-stage kidney disease (ESKD). The rate of progression depends on age, the underlying diagnosis, the implementation and success of secondary preventive measures, and the individual patient. Timely initiation of long-term renal replacement therapy is imperative to prevent the uremic complications of CKD that can lead to significant morbidity and death.
Tangri et al developed and validated a model in adult patients that uses routine laboratory results to predict progression from CKD (stages 3-5) to kidney failure. [] They reported that lower estimated glomerular filtration rate (GFR), higher albuminuria, younger age, and male sex pointed to a faster progression of kidney failure. Also, a lower serum albumin, calcium, and bicarbonate level and a higher serum phosphate level predicted an elevated risk of kidney failure. []
Unadjusted rates of hospitalization in the CKD population, reflecting its total disease burden, are 3-5 times higher than those of patients without CKD. [] After adjustment for sex, prior hospitalizations, and comorbidity, hospitalization rates for patients with CKD are 1.4 times higher. Rates of hospitalization for cardiovascular disease and bacterial infection are particularly elevated. []
In the United States in 2018, hospital admissions among patients with ESKD declined, to an average of 1.7 per patient per year. However, emergency department visits rose, to an average of 3 per patient per year. []
Hemodialysis performed 6 times per week significantly increased the risk of vascular access complications compared with a conventional 3-day regimen in one study. [] Of 125 patients who received hemodialysis 6 days per week, 48 experienced the composite primary endpoint event of vascular repair, loss, or related hospitalization, compared with only 29 of the 120 patients undergoing conventional treatment. Results indicated that overall risk for a first access event was 76% higher with daily hemodialysis than with the conventional regimen. []
The mortality rates associated with CKD are striking. After adjustment for demographics and comorbidities, deaths in 2019 in patients with and without CKD were 94.5 versus 41.5 per 1000 person-years, respectively. For patients with ESKD, the adjusted mortality rate in 2019 was 128.5 per 1000 person-years. Mortality rates rose sharply with the COVID-19 pandemic; in kidney transplant recipients, for example, mortality rates (which had decreased by nearly 5% from 2011 to 2019) increased by 34.0% in 2020 and by a further 16.3% in 2021. In the overall CKD population, however, mortality rates decreased by about 2% from 2020 to 2021. []
Mortality rates are consistently higher for men than for women, and they advance with increasing age. However, among Medicare CKD patients aged 66 years and older, the mortality rate is slightly higher for Whites than for Blacks; in 2019, deaths per 1000 patient-years were 63.2 for White patients and 58.0 for Black patients. []
The highest mortality rate is within the first 6 months of initiating dialysis. Mortality then tends to improve over the next 6 months, before increasing gradually over the next 4 years. The 5-year survival rate for a patient undergoing long-term dialysis in the United States is approximately 35%, and approximately 25% in patients with diabetes.
A study by Sens found that the risk of mortality was elevated in patients with ESKD and congestive heart failure who received peritoneal dialysis compared with those who received hemodialysis. [] Median survival time was 20.4 months in patients receiving peritoneal dialysis versus 36.7 months in the hemodialysis group.
At every age, patients with ESKD on dialysis have significantly higher mortality than nondialysis patients and individuals without kidney disease. At age 60 years, a healthy person can expect to live for more than 20 years, whereas the life expectancy of a patient aged 60 years who is starting hemodialysis is closer to 4 years. Among patients aged 65 years or older who have ESKD, mortality rates are 6 times higher than in the general population. []
The most common cause of sudden death in patients with ESRD is hyperkalemia, which often follows missed dialysis or dietary indiscretion. The most common cause of death overall in the dialysis population is cardiovascular disease; cardiovascular mortality is 10-20 times higher in dialysis patients than in the general population. []
The morbidity and mortality of dialysis patients is much higher in the United States than in most other countries, which is probably a consequence of selection bias. Because of liberal criteria for receiving government-funded dialysis in the United States and the use of rationing (medical and economic) in most other countries, US patients receiving dialysis are on the average older and sicker than those in other countries.
In the National Health and Nutrition Examination Survey (NHANES) III prevalence study, hypoalbuminemia (a marker of protein-energy malnutrition and a powerful predictive marker of mortality in dialysis patients, as well as in the general population) was independently associated with low bicarbonate, as well as with the inflammatory marker C-reactive protein. A study by Raphael et al suggests that higher serum bicarbonate levels are associated with better survival and renal outcomes in African Americans. []
A study by Navaneethan et al found a connection between low levels of 25-hydroxyvitamin D (25[OH]D) and all-cause mortality in patients with nondialysis CKD. [] Adjusted risk of mortality was 33% higher in patients whose 25(OH)D levels were below 15 ng/mL.
Morbidity and mortality among children with CKD and ESKD are much lower than among adults with these conditions, but they are strikingly higher than for healthy children. As with adults, the risk is highest among dialysis patients; consequently, transplantation is the preferred treatment for pediatric patients with ESKD.
Puberty is often delayed in boys and girls with significant CKD. Women with advanced CKD commonly develop menstrual irregularities, and those with ESKD are typically amenorrheic and infertile. However, pregnancy can occur and can be associated with accelerated renal decline, including in women with a kidney transplant. In advanced CKD and ESKD, pregnancy is associated with markedly decreased fetal survival.
Many patients with CKD have low circulating levels of 25(OH)D. A study of 1099 patients (mostly men) with advanced CKD found that the lowest tertile of 1,25(OH)(2)D (< 15 pg/mL) was associated with death and initiation of long-term dialysis therapy compared with the highest tertile (> 22 pg/mL). [] A retrospective cohort study in 12,763 non–dialysis-dependent patients with CKD found that 25(OH)D levels below 15 ng/mL were associated independently with all-cause mortality. []
Patients with chronic kidney disease (CKD) should be educated about the following:
Women of childbearing age who have end-stage kidney disease (ESKD) should be counseled that although their fertility is greatly reduced, pregnancy can occur and is associated with higher risk than in women who do not have kidney disease. In addition, many medications used to treat CKD are potentially teratogenic; in particular, women taking angiotensin-converting enzyme (ACE) inhibitors and certain immunosuppressive treatments require clear counseling.
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