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The kidney is divided into parenchyma and renal sinus. The renal sinus is hyperechoic and is composed of calyces, the renal pelvis, fat and the major intrarenal vessels. In the normal kidney, the urinary collecting system in the renal sinus is not visible, but it creates a heteroechoic appearance with the interposed fat and vessels.
The Glomerular filtration rate (GFR) is regarded as the best overall measure of the kidney's ability to carry out these numerous functions. An estimate of the GFR is used clinically to determine the degree of kidney impairment and to track the progression of the disease. The GFR, however, does not reveal the source of the kidney disease.
End-stage chronic kidney disease with increased echogenicity, homogenous architecture without visible differentiation between parenchyma and renal sinus and reduced kidney size. Measurement of kidney length on the US image is illustrated by '+' and a dashed line.
There is a great difference in echogenicity between the gas in the microbubbles and the soft tissue surroundings of the body. Thus, ultrasonic imaging using microbubble contrast agents enhances the ultrasound backscatter , (reflection) of the ultrasound waves, to produce a sonogram with increased contrast due to the high echogenicity difference.
Kidney disease usually causes a loss of kidney function to some degree and can result in kidney failure, the complete loss of kidney function. Kidney failure is known as the end-stage of kidney disease, where dialysis or a kidney transplant is the only treatment option.
Acute kidney injuries can be present on top of chronic kidney disease, a condition called acute-on-chronic kidney failure (AoCRF). The acute part of AoCRF may be reversible, and the goal of treatment, as with AKI, is to return the person to baseline kidney function, typically measured by serum creatinine .
It may cause acute kidney injury. It is now more commonly used to describe diffuse, fine, renal parenchymal calcification in radiology. [2] It is caused by multiple different conditions and is determined by progressive kidney dysfunction. These outlines eventually come together to form a dense mass. [3]
The goals of treatment are to slow the progression of kidney damage and control related complications. Management of diabetic nephropathy currently centers over four main areas: Cardiovascular risk reduction, glycemic control, blood pressure control as well as inhibition of the RAAS system. [citation needed]