University:
Western Sydney University
Course:
MEDI 2003 | Clinical Sciences 2
Academic year:

2024
Views:

203

Pages:

1
Author:

Mariam A.

Outcomes of primary and secondary glomerular disease  Determined by the pathology, and is usually identified by renal biopsy: o Resolution of Acute Phase = most likely if there is an identified cause that can be treated (e.g. acute post-streptococcal glomerulonephritis) o Response to Medical Treatment = these include corticosteroids and immunosuppressive agents. It varies from excellent response (e.g. to steroids in minimal change disease amounting to complete cure) to a limited response, possibly with no more than a slowing of the progress of the disease o Becomes Chronic = there is impairment of renal function, but this may remain stable or deteriorate slowly o Progress either rapidly or slowly to “end-stage” renal disease with total loss of homeostatic function = without intervention, death occurs in uraemia. Otherwise, the patient may require chronic haemodialysis or renal transplantation End-stage kidney disease    The causes include primary glomerular disease (esp IgA nephropathy), secondary glomerular disease (esp diabetes), non-glomerular diseases, idiopathic The renal function can be categorised as: o Severe widespread disease: acute kidney failure for days or weeks o Progressive irreversible loss of nephrons: chronic kidney failure for years o Both: eventual uraemia leading to death, dialysis or transplantation The renal pathological features include widespread loss of tubules, interstitial scarring, glomerulosclerosis and hypertensive vascular changes (features of the causal disease may be evident) o Clinical presentation: chronic renal failure – uraemia o Light microscopy: granular contracted kidney o Immunofluorescence: non-specific, with obsolete nephrons o Electron microscopy: glomerular obsolescence Terminal end-stage kidney disease – uraemia    Caused by widespread acute or chronic kidney disease, including but not limited to primary or secondary glomerular disease. The renal function is severely impaired, with complete loss of homeostatic function. This leads to multiple metabolic defects, including electrolyte and fluid imbalance and retention of nitrogenous substances (e.g. urea and creatinine). It is initially asymptomatic, but eventually becomes a systemic intoxication – uraemia. There are terminal pathological changes in the skin, heart (pericarditis), lungs (haemorrhage and oedema) and GIT (ulcerative inflammation)