Renal failure chronicN18.9

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

Chronic renal insufficiency

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DefinitionThis section has been translated automatically.

Irreversible restriction of glomerular, tubular and endocrine function of the kidneys. The dysfunctions persist over a period of > 3 months as can be proved by a glomerular filtration rate (GFR) <60ml/min/1.73qm KO.

ClassificationThis section has been translated automatically.

Chronic kidney disease is classified according to CKD stages I-V of KDIGO (Kidney Disease: Improving Global Outcome); CKD=chronic kidney disease)

  • Stage I (stage of full decompensation), GFR: > 90 (ml/min/1.73qm)
  • Stage II (stage of mild renal insufficiency), GFR: 60-89(ml/min/1.73qm)
  • Stage IIIa (stage of moderate renal insufficiency), GFR: 45-59 (ml/min/1.73qm)
  • Stage IIIb (stage of moderate renal insufficiency), GFR: 30-44 (ml/min/1.73qm)
  • Stage IV (stage of severe renal insufficiency), GFR: 15-29 (ml/min/1.73qm)
  • Stage V (stage of kidney failure), GFR: <15 (ml/min/1.73qm)

Note: the CKD stages are supplemented by the factor albuminuria. This parameter is divided into 3 degrees of severity according to A1-A3 (mg/24h). A1: <30 mg/24h; A2:30-300 mg/24h;

Glomerular filtration rate and albuminuria are independent prognostic parameters. With decreasing glomerular filtration rate and increasing albumin excretion, the risk of chronic kidney disease increases.

Occurrence/EpidemiologyThis section has been translated automatically.

Incidence in Western Europe: 10/100,000 per year (USA 60/100,000 per year)

Prevalence of chronic renal failure (glomerular filtration rate (GFR )< 60/min): 12%.

EtiopathogenesisThis section has been translated automatically.

Chronic renal insufficiency is caused by the following diseases:

  • Diabetic nephropathy (35%)
  • Primary and secondary glomerulonephritis (15%)
  • Hereditary kidney diseases, e.g. polycystic kidney generation (up to 10%)
  • Chronic tubulo-interstitial diseases
  • Vascular (hypertensive) nephropathies

Pahtogenetically, damage to individual nephrons leads to glomerular hyperinfiltration of healthy nephrons with consecutive endothelial damage and increasing glomerulosclerosis with consecutive interstitial fibrosis and tubule atrophy. The consequence is a disturbance of the excretory (retention of toxic metabolic products) and secretory function.

Clinical featuresThis section has been translated automatically.

Pale yellowish, pale (cafe-au-lait colouring) of the skin; paleness of the mucous membranes (anaemia).

Dryness of the skin, uremic pruritus (see also renal insufficiency and skin changes)

Uremic foetus

Edema (hypalbuminemia)

congestion of the lungs ("fluid lung" due to sodium and water retention)

Paresthesia (uremic polyneuropathy)

Hypertension (about 55-75% of all people with chronic renal insufficiency suffer from hypertension)

Renal osteopathy (diffuse bone pain, spontaneous fractures)

Uremic gastroenteropathy with loss of appetite and nausea

Myopathy (weakness of the proximal arm and leg muscles)

Haematological changes due to reduced production of erythropoietin (renal anaemia: normochromic, normocytic anaemia, platelet disorders with a tendency to bleed), disorders of water, electrolyte and acid-base balance, and excretory insufficiency).

Secondary hyperparathyroidism

Uremic encephalopathy

DiagnosisThis section has been translated automatically.

Medical history, clinic, laboratory, imaging procedures (sonographically small kidneys; exception chronic renal failure in systemic amyloidosis )

Differential diagnosisThis section has been translated automatically.

Differentiation of acute kidney failure.

Internal therapyThis section has been translated automatically.

Symptomatic, delaying the progression of renal insufficiency.

Treatment of the underlying disease.

Renal hypertension: ACE inhibitors, antihypertensives.

Metabolic acidosis: sodium bicarbonate, low protein, Mediterranean diet.

Hyperlipidemia: HMG-CoA reductase inhibitors.

Hypertriglyceridemia: fibrates.

Proteinuria: ACE inhibitors.

Secondary hyperparathyroidism: phosphate binders. Vit-D3 supplementation.

Cave: Potassium-sparing diuretics, inhibit the tubular potassium secretion, so that already at filtration values <50ml/min a threatening hyperkalemia can occur.

ProphylaxisThis section has been translated automatically.

People at increased risk should participate in screening activities, in particular for:

diabetes or high blood pressure,

People who are overweight,

Smokers

>-50-year-olds with a family history of diabetes, high blood pressure or kidney disease.

Note(s)This section has been translated automatically.

Healthy kidneys have a glomerular filtration rate (GFR) of 95 to 110 ml/min. This means that the kidneys filter this amount of blood per minute and cleanse it of urinary substances. With increasing renal insufficiency, the glomerular filtration rate deteriorates.

The term "terminal renal insufficiency" refers to the terminal or final stage (stage 5 according to KDIGO) of a chronic kidney disease. This terminal stage is characterized by a renal performance of 15% of the norm or less (corresponding to a GFR < 15 ml/min/1.73 m²) and by the need for renal replacement therapy in the form of dialysis treatment or kidney transplantation.

LiteratureThis section has been translated automatically.

  1. Chan IH et al (2016) Itch Management: Physical Approaches (UV Phototherapy, Acupuncture). Curr Probl Dermatol 50:54-63.
  2. Classen M et al (2004) Repetitorium Internal Medicine. Urban&Fischer Munich, Jena p.383
  3. Kremer AE et al (2016) Pruritus in systemic diseases: Common and rare etiologies. Dermatologist 67:606-614.

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Last updated on: 29.10.2020