Chronic Kidney Disease-wiki

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Chronic kidney disease

Chronic kidney disease (CKD), also known as chronic renal disease, is a progressiveloss ofrenal function over a period of months or years. The symptoms of worsening

kidney function are unspecific, and might include feeling generally unwell andexperiencing 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 highblood pressure ordiabetes and those with a blood relative with chronic kidney disease.

Chronic kidney disease may also be identified when it leads to one of its recognized

complications, such as cardiovascular disease, anemia orpericarditis.[1]

Chronic kidney disease is identified by ablood test forcreatinine (volume ofblood

plasma that is cleared of creatinine per unit time and is a useful measure for

approximating the GFR. Creatinine clearance exceeds GFR due to creatinine

secretion which can be blocked by cimetidine.). Higher levels of creatinine indicate a

falling glomerular filtration rate(describes the flow rate of filtered fluid through thekidney) 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 isdiscovered ifurinalysis (testing of a urine sample) shows that the kidney is allowing the

loss ofprotein orred blood cells into the urine. To fully investigate the underlying cause

of kidney damage, various forms ofmedical imaging, blood tests and often renalbiopsy(removing a small sample of kidney tissue) are employed to find out if there is a

reversible cause for the kidney malfunction.[1] Recent professional guidelines classify the

severity of chronic kidney disease in five stages, with stage 1 being the mildest and

usually causing few symptoms and stage 5 being a severe illness with poor lifeexpectancy if untreated. Stage 5 CKD is also called established chronic kidney disease

and is synonymous with the now outdated terms end-stage renal disease (ESRD),chronic kidney failure (CKF) orchronic renal failure (CRF).[1]

There is no specific treatment unequivocally shown to slow the worsening of chronickidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be

treated directly with treatments aimed to slow the damage. In more advanced stages,

treatments may be required for anemia andbone disease. Severe CKD requires one of theforms ofrenal replacement therapy; this may be a form ofdialysis, but ideally constitutes

a kidney transplant.[1]

Signs and symptoms

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

blood pressure is increased due to fluid overload and production of vasoactive

hormones, increasing one's risk of developing hypertension and/or suffering from

congestive heart failure
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Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging

from lethargy topericarditis and encephalopathy). Urea is excreted by sweating

and crystallizes on skin ("uremic frost").

Potassium accumulates in the blood (known as hyperkalemia with a range of

symptoms including malaise and potentially fatal cardiac arrhythmias)

Erythropoietin synthesis is decreased (potentially leading to anemia, which causesfatigue)

Fluid volume overload - symptoms may range from mild edema to life-

threateningpulmonary edema

Hyperphosphatemia - due to reduced phosphate excretion, associated with

hypocalcemia (due to vitamin D3 deficiency). The major sign of hypocalcemia

being tetany.

o Later this progresses to tertiary hyperparathyroidism, with

hypercalcaemia,renal osteodystrophy and vascular calcification that

further impairs cardiac function.

Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc.

This may cause altered enzyme activity by excess acid acting on enzymes andalso increased excitability of cardiac and neuronal membranes by the promotion

ofhyperkalemia due to excess acid (acidemia)[2]

People with chronic kidney disease suffer from accelerated atherosclerosis and are morelikely to develop cardiovascular disease than the general population. Patients afflicted

with chronic kidney disease and cardiovascular disease tend to have significantly worse

prognoses than those suffering only from the latter.

Causes

The most common causes of CKD are diabetic nephropathy,hypertension, andglomerulonephritis.[3] Together, these cause approximately 75% of all adult cases. Certain

geographic areas have a high incidence of HIV nephropathy.

Historically, kidney disease has been classified according to the part of the renal anatomy

that is involved, as:[citation needed]

Vascular, includes large vessel disease such as bilateral renal artery stenosis and

small vessel disease such as ischemic nephropathy, hemolytic-uremic syndromeand vasculitis

Glomerular, comprising a diverse group and subclassified into

o Primary Glomerular disease such as focal segmental glomerulosclerosisand IgA nephritis

o Secondary Glomerular disease such as diabetic nephropathy and lupus

nephritis

Tubulointerstitial includingpolycystic kidney disease, drug and toxin-inducedchronic tubulointerstitial nephritis and reflux nephropathy

Obstructive such as with bilateral kidney stones and diseases of the prostate
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On rare cases, pin worms infecting the kidney can also cause idiopathic

nephropathy.

Diagnosis

In many CKD patients, previous renal disease or other underlying diseases are alreadyknown. A small number presents with CKD of unknown cause. In these patients, a cause

is occasionally identified retrospectively.[citation needed]

It is important to differentiate CKD from acute renal failure (ARF) because ARF can bereversible. Abdominal ultrasound is commonly performed, in which the size of the

kidneys are measured. Kidneys with CKD are usually smaller (< 9 cm) than normal

kidneys with notable exceptions such as in diabetic nephropathy andpolycystic kidney

disease. Another diagnostic clue that helps differentiate CKD and ARF is a gradual risein 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 apatient briefly as having ARF until it has been established that the renal impairment is

irreversible.[citation needed]

Additional tests may include nuclear medicineMAG3 scan to confirm blood flows and

establish the differential function between the two kidneys. DMSA scans are also used inrenal imaging; with both MAG3 and DMSA being used chelated with the radioactive

element Technetium-99.[citation needed]

In chronic renal failure treated with standard dialysis, numerous uremic toxins

accumulate. These toxins show various cytotoxic activities in the serum, 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.[citation needed]

Stages

All individuals with a Glomerular filtration rate (GFR)


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The loss of protein in the urine is regarded as an independent marker for worsening of

renal function and cardiovascular disease. Hence, British guidelines append the letter "P"

to the stage of chronic kidney disease if there is significant protein loss.[4]

Stage 1

Slightly diminished function; Kidney damage with normal or relatively high GFR (>90

mL/min/1.73 m2). Kidney damage is defined as pathologic abnormalities or markers of

damage, including abnormalities in blood or urine test 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 pathologic abnormalities or markers of damage, including abnormalities in

blood or urine test or imaging studies.[1]

Stage 3

Moderate reduction in GFR (30-59 mL/min/1.73 m2).[1] British guidelines distinguishbetween stage 3A (GFR 45-59) and stage 3B (GFR 30-44) for purposes of screening and

referral.[4]

Stage 4

Severe reduction in GFR (15-29 mL/min/1.73 m2)[1] Preparation for renal replacementtherapy

Stage 5

Established kidney failure (GFR


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Currently, several compounds are in development for CKD. These include, but are not

limited to,bardoxolone methyl[9], olmesartan medoxomil, sulodexide, and avosentan[10].

Replacement oferythropoietin and vitamin D3, two hormones processed by the kidney, isusually necessary in patients with CKD, as is calcium. Phosphate binders are used to

control the serumphosphate levels, which are usually elevated in chronic kidney disease.

When one reaches stage 5 CKD, renal replacement therapy is required, in the form of

eitherdialysis or a transplant.

In some cases, dietary modifications have been proven to slow and even reverse furtherprogression. Generally this includes limiting protein intake.[citation needed]

The normalization of hemoglobin has not been found to be of any benefit.[11]

Prognosis

The prognosis of patients with chronic kidney disease is guarded as epidemiological datahas shown that all cause mortality (the overall death rate) increases as kidney function

decreases.[12] The leading cause of death in patients with chronic kidney disease is

cardiovascular disease, regardless of whether there is progression to stage 5.[12][13][14]

While renal replacement therapies can maintain patients indefinitely and prolong life, thequality of life is severely affected.[15][16]Renal transplantation increases the survival of

patients with stage 5 CKD significantly when compared to othertherapeutic options;[17][18]

however, it is associated with an increased short-term mortality (due to complications ofthe surgery). Transplantation aside, high intensity home hemodialysis appears to be

associated with improved survival and a greaterquality of life, when compared to theconventional three times a weekhemodialysis andperitoneal dialysis.[19]
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Afferent - are a group ofblood vessels that supply the nephrons in many excretory systems. They play an

important role in the regulation ofblood pressure as a part of the Tubuloglomerular feedbackmechanism.

Supplies blood to kidneys.

Efferent - areblood vessels that are part of the urinary tract oforganisms. The efferent arterioles form from

a convergence of the capillaries of the glomerulus. They play an important role in maintaining the

glomerular filtration rate despite fluctuations in blood pressure.

Glomerular cap - A glomerulus is a capillary tuft that performs the first step in filteringblood to form

urine.

It is surrounded by Bowman's capsule in nephrons of the vertebrate kidney. It receives its blood supplyfrom an afferent arteriole of the renal circulation. Unlike most other capillary beds, the glomerulus drains

into an efferent arteriole rather than a venule. The resistance of the arterioles results in high pressure in the

glomerulus, aiding the process ofultrafiltration, where fluids and soluble materials in the blood are forced

out of the capillaries and into Bowman's capsule.

A glomerulus and its surrounding Bowman's capsule constitute a renal corpuscle, the basic filtration unit of

the kidney. The rate at which blood is filtered through all of the glomeruli, and thus the measure of the

overall renal function, is the glomerular filtration rate (GFR).

peritubular capillaries are tiny blood vessels that travel alongside nephrons allowing reabsorption and

secretion between blood and the inner lumen of the nephron.

Ions and minerals that need to be saved in the body are reabsorbed into the peritubular capillaries

through active transport, secondary active transport, or transcytosis.

The ions that need to be excreted as waste are secreted from the capillaries into the nephron to be senttowards thebladderand out of the body.

The majority of exchange through the peritubular capillaries occurs because of chemical gradients, osmosis

andNa+ pumps. source efferent
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