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Renal azotemia (acute kidney failure) typically leads to uremia. It is an intrinsic disease of the kidney, generally the result of kidney parenchymal damage. Causes include kidney failure, glomerulonephritis, acute tubular necrosis, or other kidney disease. [3] The BUN:Cr in renal azotemia is less than 15.
Very low levels of azotemia may produce few, if any, symptoms. If the disease progresses, symptoms become noticeable (if the failure is of sufficient degree to cause symptoms). Kidney failure accompanied by noticeable symptoms is termed uraemia. [18] Symptoms of kidney failure include the following: [18] [19] [20] [21]
The term "non-dialysis-dependent chronic kidney disease" (NDD-CKD) is a designation used to encompass the status of those persons with an established CKD who do not yet require the life-supporting treatments for kidney failure known as kidney replacement therapy (RRT, including maintenance dialysis or kidney transplantation).
The various symptoms of acute kidney injury result from the various disturbances of kidney function that are associated with the disease. Accumulation of urea and other nitrogen-containing substances in the bloodstream lead to a number of symptoms, such as fatigue , loss of appetite , headache , nausea , and vomiting . [ 6 ]
Nephritic syndrome is a syndrome comprising signs of nephritis, which is kidney disease involving inflammation.It often occurs in the glomerulus, where it is called glomerulonephritis.
Actually, AKI used to be known as acute renal failure, or ARF, but AKI is a broader term that also includes subtle decreases in kidney function. Intrarenal, or sometimes intrinsic AKI, means that the AKI’s caused by the kidneys themselves, as opposed to prerenal and postrenal causes, which are upstream and downstream from the kidneys ...
Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. [1] In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine.
Uremic pericarditis is associated with azotemia, and occurs in about 6-10% of kidney failure patients. BUN is normally >60 mg/dL (normal is 7–20 mg/dL). However, the degree of pericarditis does not correlate with the degree of serum BUN or creatinine elevation. The pathogenesis is poorly understood. [2]