Chronic kidney disease

Chronic kidney disease

Uremic frost on the forehead and scalp of a young man who presented with complaints of chronic anorexia and fatigue with blood urea nitrogen and serum creatinine levels around 100 and 50 mg/dl, respectively
Classification and external resources
Specialty Nephrology
ICD-10 N18
ICD-9-CM 585.9 585.1-585.5 403
DiseasesDB 11288
MedlinePlus 000471
eMedicine article/238798
Patient UK Chronic kidney disease
MeSH D007676

Chronic kidney disease (CKD), also known as chronic renal disease, is progressive loss in kidney function over a period of months or years. The symptoms of worsening kidney function are not specific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with CKD. This disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia, pericarditis or renal osteodystrophy (the latter included in the novel term CKD-MBD).[1][2] CKD is a long-term form of kidney disease; thus, it is differentiated from acute kidney disease (acute kidney injury) in that the reduction in kidney function must be present for over 3 months. CKD is an internationally recognized public health problem affecting 5–10% of the world population.[3][4]

Chronic kidney disease is identified by a blood test for creatinine, which is a breakdown product of muscle metabolism. Higher levels of creatinine indicate a lower glomerular filtration rate and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests, and sometimes a kidney biopsy (removing a small sample of kidney tissue) are employed to find out if a reversible cause for the kidney malfunction is present.[1]

Previous professional guidelines classified the severity of CKD in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is often called end-stage kidney disease, end-stage renal disease, or end-stage kidney failure, and is largely synonymous with the now outdated terms chronic renal failure or chronic kidney failure; and usually means the patient requires renal replacement therapy, which may involve a form of dialysis, but ideally constitutes a kidney transplant. Recent international guidelines reclassified CKD based on cause, glomerular filtration rate category (G1,G2,G3a,G3b,G4 and G5), and albuminuria category (A1,A2,A3).[5]

Screening of at-risk people is important because treatments exist that delay the progression of CKD.[6] If an underlying cause of CKD, such as vasculitis, or obstructive nephropathy (blockage to the drainage system of the kidneys) is found, it may be treated directly to slow the damage. In more advanced stages, treatments may be required for anemia and kidney bone disease [also called renal osteodystrophy, secondary hyperparathyroidism or chronic kidney disease - mineral bone disorder (CKD-MBD)]. Chronic kidney disease resulted in 956,000 deaths in 2013 up from 409,000 deaths in 1990.[7]

Signs and symptoms

CKD is initially without specific symptoms and is generally only detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) represents one of the many complications of CKD. Notice the link between kidney, bone and heart in the CKD-MBD European-Dialysis-and-Transplantation (EDTA) Working Group logo

People with CKD suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with CKD and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter.[18]

Sexual dysfunction is very common in both men and women with CKD. A majority of men have a reduced sex drive, difficulty obtaining an erection, and reaching orgasm, and the problems get worse with age. A majority of women have trouble with sexual arousal, and painful menstruation and problems with performing and enjoying sex are common.[19]

Causes

The most common recognised cause of CKD is diabetes mellitus. Others include idiopathic (i.e. unknown cause, often associated with small kidneys on renal ultrasound), hypertension, and glomerulonephritis.[20] Together, these cause about 75% of all adult cases.

Historically, kidney disease has been classified according to the part of the kidney anatomy involved.[21]

Diagnosis

A 12-lead ECG of a person with CKD and a severe electrolyte imbalance: hyperkalemia (7.4 mmol/l) with hypocalcemia (1.6 mmol/l). The T-waves are peaked and the QT interval is prolonged.

Diagnosis of CKD is largely based on the clinical picture combined with the measurement of the serum creatinine level (see above).

Etiology

In many CKD patients, previous kidney disease or other underlying diseases are already known. A significant number present with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.

Differential diagnosis

It is important to differentiate CKD from acute kidney injury (AKI) because AKI can be reversible. Abdominal ultrasound, in which the size of the kidneys is measured, is commonly performed. Kidneys with CKD are usually smaller (≤ 9 cm) than normal kidneys, with notable exceptions such as in early diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD from AKI is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests), it is occasionally necessary to treat a patient briefly as having AKI until the kidney impairment has been established to be irreversible.

Work-up

Additional tests may include nuclear medicine MAG3 scan to confirm blood flow and establish the differential function between the two kidneys. Dimercaptosuccinic acid (DMSA) scans are also used in kidney imaging; with both MAG3 and DMSA being used chelated with the radioactive element technetium-99.

Toxins

In CKD numerous uremic toxins accumulate in the blood. Even when ESKD (largely synonymous with CKD5) is treated with dialysis, the toxin levels do not go back to normal as dialysis is not that efficient. Similarly, after a kidney transplant, the levels may not go back to normal as the transplanted kidney may not work 100%. If it does, the creatinine level is often normal. The toxins show various cytotoxic activities in the serum and have different molecular weights, and some of them are bound to other proteins, primarily to albumin. Such toxic protein-bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today.

Screening

Screening those who have neither symptoms nor risk factors for CKD is not recommended.[24] Those who should be screened include: those with hypertension or history of cardiovascular disease, those with diabetes or marked obesity, those aged > 60 years, subjects with indigenous racial origin, those with a history of kidney disease in the past, and subjects who have relatives who had kidney disease requiring dialysis. Screening should include calculation of estimated GFR from the serum creatinine level, and measurement of urine albumin-to-creatinine ratio (ACR) in a first-morning urine specimen (this reflects the amount of a protein called albumin in the urine), as well as a urine dipstick screen for hematuria.[25] The GFR (glomerular filtration rate) is derived from the serum creatinine and is proportional to 1/creatinine, i.e. it is a reciprocal relationship (the higher the creatinine, the lower the GFR). It reflects one aspect of kidney function: how efficiently the glomeruli (filtering units) work. But as they make up <5% of the mass of the kidney, the GFR does not tell you about all aspects of kidney health and function. This can be done by combining the GFR level with the clinical assessment of the patient (especially fluid state) and measuring the levels of hemoglobin, potassium, phosphate and parathyroid hormone (PTH). Normal GFR is 90-120 mls/min. The units of creatinine vary from country to country.

Referral to nephrologist

Guidelines for referral to a nephrologist vary between countries. Though most would agree that nephrology referral is required by Stage 4 CKD (when eGFR/1.73m2 is less than 30 ml/min; or decreasing by more than 3 ml/min/year); and may be useful at an earlier stage (e.g. CKD3) when urine albumin-to-creatinine ratio is more than 30 mg/mmol, when blood pressure is difficult to control, or when hematuria or other findings suggest either a primarily glomerular disorder or secondary disease amenable to specific treatment. Other benefits of early nephrology referral include proper patient education regarding options for renal replacement therapy as well as pre-emptive transplantation, and timely workup and placement of an arteriovenous fistula in those patients opting for future hemodialysis

Severity-based stages

CKD Stage GFR level (mL/min/1.73 m2)
Stage 1 ≥ 90
Stage 2 60 – 89
Stage 3 30 – 59
Stage 4 15 – 29
Stage 5 < 15

All individuals with a glomerular filtration rate (GFR) <60 ml/min/1.73 m2 for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications such as the development of cardiovascular disease.[1]

The loss of protein in the urine is regarded as an independent marker for worsening of kidney function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if protein loss is significant.[26]

Stage 1

Slightly diminished function; kidney damage with normal or relatively high GFR (≥90 ml/min/1.73 m2). Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.[1]

Stage 2

Mild reduction in GFR (60–89 ml/min/1.73 m2) with kidney damage. Kidney damage is defined as pathological abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.[1]

Stage 3

Moderate reduction in GFR (30–59 ml/min/1.73 m2):.[1] British guidelines distinguish between stage 3A (GFR 45–59) and stage 3B (GFR 30–44) for purposes of screening and referral.[26]

Stage 4

Severe reduction in GFR (15–29 ml/min/1.73 m2)[1] Preparation for renal replacement therapy.

Stage 5

Established kidney failure (GFR <15 ml/min/1.73 m2), permanent renal replacement therapy,[1] or end-stage kidney disease.

NDD-CKD vs. ESRD

The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as renal replacement therapy (RRT, including maintenance dialysis or kidney transplantation). The condition of individuals with CKD, who require either of the two types of renal replacement therapy (dialysis or transplant), is referred to as the end-stage kidney disease (ESKD). Hence, the start of the ESKD is practically the irreversible conclusion of the NDD-CKD. Even though the NDD-CKD status refers to the status of persons with earlier stages of CKD (stages 1 to 4), patients with advanced stage of CKD (stage 5), who have not yet started renal replacement therapy, are also referred to as NDD-CKD.

Treatment

The presence of CKD confers a markedly increased risk of cardiovascular disease, and people with CKD often have other risk factors for heart disease, such as high blood lipids. The most common cause of death in people with CKD is cardiovascular disease rather than kidney failure. Aggressive treatment of hyperlipidemia is warranted.[27]

Apart from controlling other risk factors, the goal of therapy is to slow down or halt the progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs) are used, as they have been found to slow the progression of CKD to kidney failure.[28] They have also been found to reduce the risk of major cardiovascular events such as myocardial infarction, stroke, heart failure, and death from cardiovascular disease when compared to placebo in individuals with CKD.[28] Furthermore, ACEIs may be superior to ARBs for protection against progression to kidney failure and death from any cause in those with CKD.[28]

Although the use of ACE inhibitors and ARBs represents the current standard of care for people with CKD, people progressively lose kidney function while on these medications, as seen in the IDNT[29] and RENAL[30] studies, which reported a decrease over time in estimated GFR (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines[1]) in people treated by these conventional methods.

Replacement of erythropoietin and calcitriol, two hormones processed by the kidney, is often necessary in people with advanced disease. Guidelines[31] recommend treatment with parenteral iron prior to treatment with erythropoietin. A target hemoglobin level of 9–12 g/dl is recommended.[32][33] The normalization of hemoglobin has not been found to be of benefit.[34] It is unclear if androgens help with anemia.[35] Phosphate binders are also used to control the serum phosphate levels, which are usually elevated in advanced chronic kidney disease. Although the evidence for them is limited, phosphodiesterase-5 inhibitors and zinc show potential for helping men with sexual dysfunction.[19]

At stage 5 CKD, renal replacement therapy is usually required, in the form of either dialysis or a transplant.

Prognosis

The prognosis of patients with chronic kidney disease is guarded as epidemiological data have shown that all cause mortality (the overall death rate) increases as kidney function decreases.[36] The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5.[36][37][38]

While renal replacement therapies can maintain patients indefinitely and prolong life, the quality of life is severely affected.[39][40] Kidney transplantation increases the survival of patients with stage 5 CKD significantly when compared to other therapeutic options;[41][42] however, it is associated with an increased short-term mortality due to complications of the surgery. Transplantation aside, high-intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three-times-a-week hemodialysis and peritoneal dialysis.[43]

Cancer risk

Patients with ESKD are at increased overall risk for cancer.[44] This risk is particularly high in younger patients and gradually diminishes with age.[44] Medical specialty professional organizations recommend that physicians do not perform routine cancer screening in patients with limited life expectancies due to ESKD because evidence does not show that such tests lead to improved patient outcomes.[45][46]

Epidemiology

Chronic kidney disease resulted in 956,000 deaths in 2013 up from 409,000 deaths in 1990.[7]

In Canada, 1.9 to 2.3 million people have CKD.[34] The U.S. Centers for Disease Control and Prevention found that CKD affected an estimated 16.8% of U.S. adults aged 20 years and older, during 1999 to 2004.[47] UK estimates suggest that 8.8% of the population of Great Britain and Northern Ireland have symptomatic CKD.[48]

CKD is a major concern in African Americans, mostly due to increased prevalence of hypertension. As an example, 37% of ESKD cases in African Americans can be attributed to high blood pressure, compared with 19% among Caucasians.[49] Treatment efficacy also differs between racial groups. Administration of antihypertensive drugs generally halts disease progression in white populations, but has little effect in slowing kidney disease among blacks, and additional treatment such as bicarbonate therapy is often required.[49] While lower socioeconomic status contributes to prevalence of CKD, significant differences in CKD prevalence are still evident between African Americans and Whites when controlling for environmental factors.[49]

Studies have shown a true association between history of chronic kidney disease in first- or second-degree relatives, and risk of disease.[50] In addition, African Americans may have higher serum levels of human leukocyte antigens (HLA).[50] High HLA concentrations can contribute to increased systemic inflammation, which indirectly may lead to heightened susceptibility for developing kidney disease. Lack of nocturnal reduction in blood pressure among groups of African Americans is also offered as an explanation,[50] which lends further credence to a genetic etiology of CKD racial disparities.

A high and so-far unexplained incidence of CKD, referred to as the Mesoamerican nephropathy, has been noted among male workers in Central America, mainly in sugar cane fields in the lowlands of El Salvador and Nicaragua. Heat stress from long hours of piece-rate work at high average temperatures[51][52][53][54] (in the range of 96 °F) is suspected, as are agricultural chemicals[55][56] and other factors. In Sri Lanka, another epidemic of CKD of unknown etiology has become a serious public health concern.[22]

Society and culture

In the USA, the National Kidney Foundation is a national organization representing patients and professionals who treat kidney diseases. The American Kidney Fund is a national nonprofit organization providing treatment-related financial assistance to one of every five dialysis patients each year. The Renal Support Network is a nonprofit, patient-focused, patient-run organization that provides nonmedical services to those affected by CKD. The American Association of Kidney Patients is a nonprofit, patient-centric group focused on improving the health and well-being of CKD and dialysis patients. The Renal Physicians Association is an association representing nephrology professionals.

In the United Kingdom, the UK National Kidney Federation and British Kidney Patient Association (BKPA) represents patients, and the Renal Association represents renal physicians and works closely with the National Service Framework for kidney disease.

Kidney Health Australia

serves that country.

The International Society of Nephrology is an international body representing specialists in kidney diseases.

Research

Currently, several compounds are in development for the treatment of CKD. These include the angiotensin receptor blocker (ARB) olmesartan medoxomil [citation needed]; and sulodexide, a mixture of low molecular weight heparin and dermatan sulfate [citation needed].

References

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  2. 1 2 3 4 KDIGO: Kidney Disease Improving Global Outcomes (August 2009). "KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)" (PDF). Kidney Int 76 (Suppl 113).
  3. ↑ Eknoyan G, Lameire N, Barsoum R; et al. (2004). "The burden of kidney disease: improving global outcomes". Kidney Int 66: 1310–4. doi:10.1111/j.1523-1755.2004.00894.x. PMID 15458424.
  4. ↑ A Martínez-Castelao, JL. Górriz, J Bover; et al. (2014). "Consensus document for the detection and management of chronic kidney disease". Nefrologia 34 (2): 243–62. doi:10.3265/Nefrologia.pre2014.Feb.12455. PMID 4658201.
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  9. ↑ Hruska KA, Mathew S, Lund R, Qiu P, Pratt R (2008). "Hyperphosphatemia of chronic kidney disease". Kidney Int. 74 (2): 148–57. doi:10.1038/ki.2008.130. PMC 2735026. PMID 18449174.
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