Glomerulosclerosis

from Wikipedia, the free encyclopedia
Classification according to ICD-10
N26 Shrunken kidney, unspecified
ICD-10 online (WHO version 2019)
Glomeruloesclerosi.1445.jpg

The glomerulosclerosis (of glomerulus and ancient Greek σκληρός skleros "hard") is contrary to glomerulonephritis not flammable conditional part of Glomerulopathies .

The hardening is caused by scarring (sclerosis) of the capillary loops of the kidney corpuscles with proliferation and increase in thickness of the connective tissue as a result of all diseases with a loss of kidney tissue, often with high blood pressure and diabetes mellitus .

The main symptom is the development of a nephrotic syndrome .

distribution

Glomerulosclerosis occurs in up to 20% of diabetics, especially those with poor blood sugar control .

About 15% of all proteinurias are caused by glomerulosclerosis.

The disease can occur at any age. Even in the case of chronification , it is basically reversible , often only temporarily.

root cause

Common causes are diabetes mellitus, as well as toxins , drugs or infections (e.g. HIV infection ).

pathology

The pathomechanism of glomerulosclerosis, formerly also known as "hypertonic nephrosis of the diabetic", is complex:

Put simply, the reduction in functional nephrons leads to glomerular hypertrophy and arterial hypertension , both of which lead to the proliferation of mesangial cells . Additional factors are the accumulation of lipids with macrophage activation , a toxic-related hyperfiltration of macromolecules with changes in the extracellular matrix as well as vascular damage to the endothelium with microthrombi .

Classification

According to clinical criteria, the following forms can be distinguished:

Clinical manifestations

The only early symptom is painless proteinuria, later it comes to nephrotic syndrome, and if left untreated, chronic kidney failure can develop.

literature

  • R. Wanke, E. Wolf, G. Brem, W. Hermanns: On the importance of podocyte damage in the pathogenesis of glomerulosclerotic and tubulointerstitial lesions: Findings obtained using the model of progressive nephropathy in growth hormone-transgenic mice. In: Negotiations of the German Society for Pathology , Volume 85, 2001, pp. 250-256, PMID 11894406 .
  • M. Teschner, A. Heidland: The reduced intrarenal protein degradation as an alternative mediator of glomerulosclerosis and tubulointerstitial fibrosis In: Medical Clinic (Munich, Germany: 1983). Volume 95, No. 7, July 2000, pp. 385-391, PMID 10943099 (review).
  • S. Chandragiri, S. Raju, KK Mukku, S. Babu, MS Uppin: Idiopathic nodular glomerulosclerosis: Report of two cases and review of literature. In: Indian journal of nephrology , Volume 26, No. 2, 2016 Mar-Apr, pp. 145-148, doi: 10.4103 / 0971-4065.164233 , PMID 27051142 , PMC 4795433 (free full text).

Web links

Individual evidence

  1. ^ Claus-Peter Adler, Ursus-Nikolaus Riede: General and special pathology . Thieme, Stuttgart a. a. 1993, ISBN 3-13-778701-7 .
  2. Nutrition Lexicon
  3. a b c Willibald Pschyrembel : Clinical Dictionary , 266th edition, de Gruyter , Berlin 2014, ISBN 978-3-11-033997-0 , keyword glomerulosclerosis .
  4. ^ Joachim Frey : Glomerulosclerosis. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition ibid. 1961, pp. 957 f.
  5. M. Tepel, M. van der Giet, W. Zidek: Practical therapy of chronic renal insufficiency through progression inhibition. In: Deutsches Ärzteblatt , Volume 94, No. 41, 1997, pages A-2648-2652.
  6. ^ S. Chandragiri, S. Raju, KK Mukku, S. Babu, MS Uppin: Idiopathic nodular glomerulosclerosis: Report of two cases and review of literature. In: Indian journal of nephrology , Volume 26, Number 2, 2016 Mar-Apr, pp. 145-148, doi: 10.4103 / 0971-4065.164233 , PMID 27051142 , PMC 4795433 (free full text).