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Alterations in renal function and structure are found even at the onset of diabetes mellitus.

Studies performed over the last decade now allow definition of a series of stages in the development of renal changes in diabetes. Such a classification may be useful both in clinical work and in research activities. Stage 1 is characterized by early hyperfunction and hypertrophy. These changes are found at diagnosis, before insulin treatment. Increased urinary albumin excretion, aggravated during physical exercise, is also a characteristic finding. Changes are at least partly reversible by insulin treatment. Stage 2 develops silently over many years and is characterized by morphologic lesions without signs of clinical disease. However, kidney function tests and morphometry on biopsy specimens reveal changes. The function is characterized by increased GFR. During good diabetes control, abumin excretion is normal; however, physical exercise unmasks changes in albuminuria not demonstrable in the resting situation. During poor diabetes control albumin excretion goes up both at rest and during exercise. A number of patients continue in stage 2 throughout their lives. Stage 3, incipient diabetic nephropathy, is the forerunner of overt diabetic nephropathy. Its main manifestation is abnormally elevated urinary albumin excretion, as measured by radioimmunoassay. A level higher than the values found in normal subjects but lower than in clinical disease is the main characteristic of this stage, which appeared to be between 15 and 300 g/min in the baseline situation. A slow, gradual increase over the years is a prominent feature in this very decisive phase of renal disease in diabetes when blood pressure is rising. The increased rate in albumin excretion is higher in patients with increased blood pressure. GFR is still supranormal and antihypertensive treatment in this phase is under investigation, using the physical exercise test. Stage 4 is overt diabetic nephropathy, the classic entity characterized by persistent proteinuria (>0.5 g/ 24 h). When the associated high blood pressure is left untreated, renal function (GFR) declines, the mean fall rate being around 1 ml/min/mo. Long-term antihypertensive treatment reduces the fall rate by about 60% 7 and thus postpones uremia considerably. Stage 5 is end-stage renal failure with uremia due to diabetic nephropathy. As many as 25% of the population presently entering the end-stage renal failure programs in the United States are diabetic. Diabetic nephropathy and diabetic vasculopathy constitute a major medical problem in society today. End-stage kidney disease

Email this page to a friendShare on facebookShare on twitterBookmark & SharePrinter-friendly version End-stage kidney disease is the complete or almost complete failure of the kidneys to work. The kidneys remove waste and excess water from the body. Causes End-stage kidney disease (ESRD) is when the kidneys are no longer able to work at a level needed for day-to-day life. The most common causes of ESRD in the U.S. are diabetes and high blood pressure. These conditions can affect your kidneys. ESRD almost always comes after chronic kidney disease. The kidneys may slowly stop working over 10 - 20 years before end-stage disease results. Symptoms Symptoms may include:

General ill feeling and fatigue Itching (pruritus) and dry skin Headaches Weight loss without trying Loss of appetite Nausea

Other symptoms may include:

Abnormally dark or light skin Nail changes Bone pain Drowsiness and confusion Problems concentrating or thinking Numbness in the hands, feet, or other areas Muscle twitching or cramps Breath odor Easy bruising, nosebleeds, or blood in the stool Excessive thirst Frequent hiccups Low level of sexual interest and impotence Menstrual periods stop (amenorrhea) Sleep problems, such as insomnia, restless leg syndrome, or obstructive sleep apnea Swelling of the feet and hands (edema) Vomiting, especially in the morning

Exams and Tests Your health care provider will perform a physical exam and order blood tests. Most people with this condition have high blood pressure. Patients with end-stage kidney disease will make much less urine, or urine production may stop. End-stage kidney disease changes the results of many tests. Patients receiving dialysis will need these and other tests done often:

Potassium Sodium Albumin Phosphorous Calcium Cholesterol Magnesium Complete blood count (CBC) Electrolytes

This disease may also change the results of the following tests:

Erythropoietin PTH Bone density test

Treatment Dialysis or kidney transplantation is the only treatment for this condition. For more information on these treatments, see:

Dialysis Kidney transplant

Your doctor may also put you on medicine to control your blood pressure. You may need to make changes in your diet.

Eat a low-protein diet Get enough calories if you are losing weight Limit fluids Limit salt, potassium, phosphorous, and other electrolytes

For more information, see: Diet and chronic kidney disease

Other treatment depends on your symptoms but may include:

Extra calcium and vitamin D (always talk to your doctor before taking) Medicines called phosphate binders, to help prevent phosphorous levels from becoming too high Treatment for anemia, such as extra iron in the diet, iron pills or shots, shots of a medicine called erythropoietin, and blood transfusions.

You should be up-to-date on important vaccinations, including:

H1N1 (swine flu) vaccine Hepatitis A vaccine Hepatitis B vaccine Influenza vaccine Pneumococcal polysaccharide vaccine (PPV)

Support Groups See: Kidney disease support group Outlook (Prognosis) End-stage kidney disease leads to death if you do not have dialysis or a kidney transplant. However, both of these treatments can have risks. The outcome is different for each person. Possible Complications

Anemia Bleeding from the stomach or intestines Bone, joint, and muscle pain Brain dysfunction, confusion, and dementia Changes in electrolyte levels Changes in blood sugar (glucose) Damage to nerves of the legs and arms Fluid buildup around the lungs Heart and blood vessel complications o Congestive heart failure o Coronary artery disease o High blood pressure o Pericarditis o Stroke Hepatitis B, hepatitis C, liver failure Hyperparathyroidism Increased risk of infections Malnutrition Phosphorous levels become too high

Potassium levels become too high Seizures Skin dryness, itching/scratching, leading to skin infection Weakening of the bones, fractures, joint disorders

Prevention Treatment of chronic kidney disease may delay or prevent progression to ESRD. Some cases may not be preventable. Alternative Names Renal failure - end stage; Kidney failure - end stage; ESRD BSTRACT. Diabetic nephropathy (DN), a major cause of ESRD, is undoubtedly multifactorial and is caused by environmental and genetic factors. To identify a genetic basis for DN susceptibility, we are collecting multiplex DN families in the Caucasian (CA) and AfricanAmerican (AA) populations for whole genome scanning and candidate gene analysis. A candidate gene search of diabetic sibs discordantly affected, concordantly affected and concordantly unaffected for DN was performed with microsatellite markers in genomic regions suspected to harbor nephropathy susceptibility loci. Regions examined were at human chromosome 10p,10q (orthologous to the rat renal susceptibility Rf-1 locus), and at NPHS1 (nephrin), CD2AP, Wilms tumor (WT1), and NPHS2 (podocin) loci. Linkage analyses were conducted using model-free methods (SIBPAL, S.A.G.E.) for AA, CA, and the combined sample. Allele frequencies and the identity by descent sharing were estimated separately for AA and CA, and race was included as a covariate in the final linkage analysis. To date, we have collected 212 sib pairs from 46 CA and 50 AA families. The average age of diabetes onset was 46.8 yrversus 36.2 yr for CA and 39.5 yr versus 40.2 yr for AA, in males versus females respectively. Genotyping data were available for 106 sib pairs (43 CA, 63 AA) from 27 CA (44% male probands) and 38 AA families (43% male probands). Average AA and CA sibship size was 2.73. Singlepoint and multipoint linkage analyses indicate that marker D10S1654 on chromosome 10p is potentially linked to DN (CA only multipoint P = 4 103). Interestingly, the majority of the linkage evidence derives from the CA sib pairs. We are now adding sib pairs and increasing marker density on chromosome 10. We have excluded linkage with candidate regions for nephrin, CD2AP, WT1, and podocin in this sample. In conjunction with previous reports, our data support evidence for a DN susceptibility locus on chromosome 10. E-mail: 20