The negative feedback loop for glucocorticoids Causes of<unk> renal insufficiency can be categorized by the mechanism through which they cause the<unk> renal glands to produce insufficient cortisol. This can be due to damage or destruction of the<unk> renal cortex. These deficiencies include glucocorticoid and mineralocorticoid hormones as well. These are<unk> renal dysgenesis (the gland has not formed<unk> equately during development), impaired steroidogenesis (the gland is present but is biochemically unable to produce cortisol), or<unk> renal destruction (disease processes leading to glandular damage).<unk> renal destruction Autoimmune<unk> renalitis is the most common cause of<unk>  in the industrialized world. Autoimmune destruction of the<unk> renal cortex is caused by an immune reaction against the enzyme 21-hydroxylase (a phenomenon first described in 1992). This may be isolated or in the context of autoimmune polyendocrine syndrome (APS type 1 or 2), in which other hormone-producing organs, such as the thyroid and pancreas, may also be affected.<unk> renal destruction is also a feature of<unk> renoleukodystrophy, and when the<unk> renal glands are involved in metastasis (seeding of cancer cells from elsewhere in the body, especially lung), hemorrhage (e.g., in Waterhouse–Friderichsen syndrome or antiphospholipid syndrome), particular infections (tuberculosis, histoplasmosis, coccidioidomycosis), or the deposition of abnormal protein in amyloidosis.<unk> renal dysgenesis All causes in this category are genetic, and generally very rare. These include mutations to the SF1 transcription factor, congenital<unk> renal hypoplasia due to DAX-1 gene mutations and mutations to the ACTH receptor gene (or related genes, such as in the Triple-A or Allgrove syndrome). DAX-1 mutations may cluster in a syndrome with glycerol kinase deficiency with a number of other symptoms when DAX-1 is deleted together with a number of other genes. Impaired steroidogenesis To form cortisol, the<unk> renal gland requires cholesterol, which is then converted biochemically into steroid hormones. Interruptions in the delivery of cholesterol include Smith–Lemli–Opitz syndrome and abetalipoproteinemia. Of the synthesis problems, congenital<unk> renal hyperplasia is the most common (in various forms: 21-hydroxylase, 17α-hydroxylase, 11β-hydroxylase and 3β-hydroxysteroid dehydrogenase), lipoid CAH due to deficiency of StAR and mitochondrial DNA mutations. Some medications interfere with steroid synthesis enzymes (e.g., ketoconazole), while others accelerate the normal breakdown of hormones by the liver (e.g., rifampicin, phenytoin).
Addison's disease
Sheehan's syndrome
Cushing's disease
Wilson's temperature syndrome
Sneddon's syndrome
complications of Acromegaly
Zieve's syndrome
Young's syndrome