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Acute tubular necrosis
Renal cortical necrosis
Renal papillary necrosis
IgA nephropathy (NORD)
Rapidly progressive glomerulonephritis
Focal segmental glomerulosclerosis (NORD)
Minimal change disease
Medullary cystic kidney disease
Medullary sponge kidney
Multicystic dysplastic kidney
Polycystic kidney disease
Chronic kidney disease
Renal tubular acidosis
Nephroblastoma (Wilms tumor)
Renal cell carcinoma
Renal artery stenosis
Acid-base disturbances: Pathology review
Congenital renal disorders: Pathology review
Electrolyte disturbances: Pathology review
Kidney stones: Pathology review
Nephritic syndromes: Pathology review
Nephrotic syndromes: Pathology review
Renal and urinary tract masses: Pathology review
Renal failure: Pathology review
Renal tubular acidosis: Pathology review
Renal tubular defects: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Chronic kidney disease
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|Blood urea nitrogen||70 mg/dL|
|Serum 25-OH Vitamin D (D2)||45 ng/mL (normal: 25-80 ng/mL)|
|Serum 1,25-OH Vitamin D (D3)||30 pg/mL (normal: 18-64 pg/mL)|
in anemia taxonomy p. 425
erythropoietin in p. 613
hypertension and p. 306
hypherphosphatemia with p. 344
chronic renal failure and p. 627
Now the kidney’s job is to regulate what’s in the blood, so they might remove waste, or make sure electrolyte levels are steady, or regulate the overall amount of water, and even make hormones - the kidneys do a lot of stuff!
Blood gets into the kidney through the renal artery, and once inside it goes gets into tiny clumps of arterioles called glomeruli where it’s initially filtered, and the filtrate which is the stuff that gets filtered out, moves into the renal tubule.
The rate at which this filtration takes place is known as glomerular filtration rate or GFR. In a normal healthy person, this is somewhere around 100-120 milliliter of fluid filtered per minute per 1.73 m2 of body surface area. The value is slightly less in women than men and it decreases slowly in all of us as we grow older.
In hypertension, the walls of arteries supplying the kidney begin to thicken in order to withstand the pressure, and that results in a narrow lumen. A narrow lumen means less blood and oxygen gets delivered to the kidney, resulting in ischemic injury to the nephron’s glomerulus.
These growth factors cause the mesangial cells to regress back to their more immature stem cell state known as mesangioblasts and secrete extracellular structural matrix. This excessive extracellular matrix leads to glomerulosclerosis, hardening and scarr, and diminishes the nephron’s ability to filter the blood - over time leading to chronic kidney disease.
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