Nephrosclerosis

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Classification according to ICD-10
I12.0 Hypertensive kidney disease with renal insufficiency
I12.9 Hypertensive kidney disease without renal insufficiency
ICD-10 online (WHO version 2019)

As nephrosclerosis (also hypertensive nephropathy ) is defined as a non-inflammatory kidney disease ( nephropathy ) as a result of high blood pressure ( hypertension ) associated with an increased protein excretion in the urine ( proteinuria to renal impairment () is accompanied and renal failure may result).

classification

In the ICD-10 , hypertensive nephropathy without renal insufficiency is coded with I12.9, with renal insufficiency as I12.0, whereby existing multiple diseases have complex effects on this coding.

The benign (benign) nephrosclerosis runs over years or decades and is characterized by proliferation of connective tissue (fibrosis) , scarring (sclerosis) and storage transparent substances (hyalinosis) in the range of arteries , arterioles (smallest arteries), glomeruli , renal tubules (tubules) and intermediate tissue (Interstitium).

The malignant (malignant) nephrosclerosis (also called "primary genuine Nephrozirrhose" and "arteriosclerotic contracted kidney ") can very quickly to kidney failure cause. It is characterized by an increase in smooth muscle cells in the innermost layer (intima) of the arteries (myointimal proliferation ).

Classification according to ICD-10
I12.0 Hypertensive kidney disease with renal insufficiency
I12.9 Hypertensive kidney disease without renal insufficiency
ICD-10 online (WHO version 2019)

As nephrosclerosis (also hypertensive nephropathy ) is defined as a non-inflammatory kidney disease ( nephropathy ) as a result of high blood pressure ( hypertension ) associated with an increased protein excretion in the urine ( proteinuria to renal impairment () is accompanied and renal failure may result).

A distinction is often made between three stages:

  1. Microalbuminuria (20–200 mg albumin per liter urine or 30–300 mg per day),
  2. Benign hypertensive nephrosclerosis with albuminuria (> 300 mg per day) and
  3. Arterio-arteriolosclerotic shrunken kidneys with renal insufficiency.

Pathogenesis

In the kidney corpuscles , increased blood pressure leads to the upregulation of Ras homolog gene family, member A (RhoA) of a small GTP-ase from the RAS superfamily . Caveolae and caveolin-1 play an important role in transmitting mechanical stress signals. The upregulation of RhoA leads to increased production of extracellular matrix and this in turn is an important mechanism for the development of nephrosclerosis.

genetics

Nephrosclerosis is around four times more common in people of black African descent than in white people. In addition, in black Africans, the progression of impaired kidney function cannot be prevented so well even by good blood pressure control. A lack of nocturnal blood pressure drop and genetic factors are assumed to be the cause. Several single nucleotide polymorphisms in the gene for the non-muscle myosin myosin MYH9 heavy chain were found to be associated with an increased risk of chronic kidney disease (especially nephrosclerosis and focal segmental glomerulosclerosis ). MYH9 itself is probably not responsible for the increased risk , but rather the directly neighboring gene APOL1 . Variants of this gene give the carriers a resistance to infections with Trypanosoma brucei rhodesiense and thus a selection advantage . The APOL1 gene codes for the protein apolipoprotein LI (APOL1), which was only found in humans and gorillas. When trypanosomes ingest APOL1 through endocytosis , APOL1 forms pores in the membrane of the lysosomes , which lead to lysis of the parasite cells. The pathomechanism by which APOL1 leads to kidney damage in humans is not yet known. A classic example of this selection mechanism is the sickle cell anemia gene , which gives heterozygous carriers resistance to malaria .

Epidemiology and economic significance

The number of new cases (incidence) of nephrosclerosis has increased significantly in recent years. In Germany in 2005, nephrosclerosis was the second most common cause of newly occurring kidney failure requiring dialysis , with a share of 23% ; in the USA, the share is 30%. The frequency of nephrosclerosis increases with age. The health care costs associated with treating high blood pressure-only kidney failure, which requires dialysis, run to $ 1 billion a year in the US; Based on the figures for Germany, one must assume around 450 million euros per year.

Risk factors

A variety of risk factors influence the occurrence (manifestation) and progression (progression) of nephrosclerosis:

Symptoms

Benign nephrosclerosis is slow to progress. Symptoms often do not appear until the stage of advanced kidney failure is reached. Symptoms of malignant nephrosclerosis occur when severe high blood pressure causes damage to the kidneys, brain, and heart. Among other things, this can lead to blurred vision, headaches, states of confusion, indifference, nausea, vomiting and coma . Seizures and heart failure can even occur.

diagnosis

Histological findings in nephrosclerosis

The definition of nephrosclerosis is based on histological (fine tissue) findings, which require a kidney biopsy (kidney puncture) to obtain kidney tissue. As a rule, however, a kidney biopsy is not performed in patients with suspected nephrosclerosis, as this is fraught with potential complications and therapy (treatment) can also be carried out without knowledge of the tissue findings.

In everyday clinical practice, the diagnosis is made on the basis of anamnesis ( medical history ), physical examination , blood and urine tests .

therapy

The treatment is carried out by lowering high blood pressure with drugs. If there is an increased excretion of protein in the urine (proteinuria) , an ACE inhibitor or an AT1 antagonist are recommended as the first choice . With normal excretion of protein in the urine, the treatment does not differ from the commonly used high-pressure treatment . If kidney function is impaired or protein excretion is increased, blood pressure should be lowered to values ​​below 130/80 mmHg at rest. With normal kidney function and normal protein excretion, lowering the blood pressure to values ​​below 140/90 mmHg is recommended; lowering the blood pressure to lower values ​​has no additional benefit.

Web links

Individual evidence

  1. ↑ Nephrosclerosis . Penn State Milton S. Hershey Medical Center Health & Disease Information.
  2. ^ Robert B Toto: Nephrology Forum - Hypertensive nephrosclerosis in African Americans . In: Kidney International , 2003, 64, pp. 2331-2341, doi: 10.1046 / j.1523-1755.2003.00333.x .
  3. ↑ Causality and complexity in multiple diagnoses and their effect on the ICD-10 coding using the example of hypertension and its secondary diseases . Straub et al; 50th annual meeting of the German Society for Medical Informatics, Biometry and Epidemiology (gmds).
  4. ↑ Joachim Frey : Diseases of the kidneys, the water and salt balance, the urinary tract and the male sexual organs. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid 1961, pp. 893-996, here: pp. 965-968 ( nephroscleroses ).
  5. ↑ ERSP Caetano: Hypertensive nephrosclerosis as a Relevant Cause of Chronic Renal Failure . In: Hypertension , 2001, 38, p. 171.
  6. ↑ Nephrosclerosis . Penn State Milton S. Hershey Medical Center Health & Disease Information
  7. ^ Robert B Toto: Nephrology Forum - Hypertensive nephrosclerosis in African Americans . In: Kidney International , 2003, 64, pp. 2331-2341, doi: 10.1046 / j.1523-1755.2003.00333.x .
  8. ↑ Fangfang Peng et al .: RhoA Activation in Mesangial Cells by Mechanical Strain Depends on Caveolae and Caveolin-1 Interaction . In: J Am Soc Nephrol . No. 18 , 2007, p. 189-198 ( article abstract ).
  9. ↑ Lawrence J. Appel, et al .: Long-term effects of renin-angiotensin system-blocking therapy and a low blood pressure goal on progression of hypertensive chronic kidney disease in African Americans . In: Archives of Internal Medicine . 168, No. 8, April 28, 2008, ISSN  1538-3679 , pp. 832-839. doi : 10.1001 / archinte.168.8.832 . PMID 18443258 .
  10. ^ WH Linda Kao, et al .: MYH9 is associated with nondiabetic end-stage renal disease in African Americans . In: Nature Genetics . 40, No. 10, October 2008, ISSN  1546-1718 , pp. 1185-1192. doi : 10.1038 / ng.232 . PMID 18794854 .
  11. ↑ Jeffrey B. Kopp, et al .: MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis . In: Nature Genetics . 40, No. 10, October 2008, ISSN  1546-1718 , pp. 1175-1184. doi : 10.1038 / ng.226 . PMID 18794856 .
  12. ^ Giulio Genovese, et al .: Association of trypanolytic ApoL1 variants with kidney disease in African Americans . In: Science . 329, No. 5993, August 13, 2010, ISSN  1095-9203 , pp. 841-845. doi : 10.1126 / science.1193032 . PMID 20647424 .
  13. ↑ E. Pays, B. Vanhollebeke, L. Vanhamme, F. Paturiaux-Hanocq, DP Nolan, D. Pérez-Morga: The trypanolytic factor of human serum. In: Nat Rev Microbiol . 2006 Jun; 4 (6), pp. 477-486, PMID 16710327
  14. ↑ U. Frei, H.-J. Schober-Halstenberg: Renal replacement therapy in Germany. In: QuaSi-Niere annual report 2005/2006 , Berlin. The data were provided by QuaSi-Niere gGmbH. The author is solely responsible for the interpretation and further evaluation of this data.
  15. ↑ JT Jr. Wright et al .: Effect of blood pressure lowering and antihypertensive drug class on progression of hypertensive kidney disease: results from the AASK trial. In: JAMA , 2002, 288, p. 2421.