Causes of decreased and increased glomerular filtration rate

Glomerular filtration rate (GFR) is a sensitive indicator of the functional state of the kidneys; its decrease is considered one of the early symptoms of renal dysfunction. A decrease in GFR, as a rule, occurs much earlier than a decrease in the concentration function of the kidneys and the accumulation of nitrogenous waste in the blood. In primary glomerular lesions, insufficiency of the concentration function of the kidneys is detected with a sharp decrease in GFR (by approximately 40-50%). In chronic pyelonephritis, the distal part of the tubules is predominantly affected, and filtration decreases later than the concentration function of the tubules. Impaired concentration function of the kidneys and sometimes even a slight increase in the content of nitrogenous waste in the blood in patients with chronic pyelonephritis is possible in the absence of a decrease in GFR.

Extrarenal factors influence the SCF. Thus, the SCF decreases in cardiac and vascular failure, profuse diarrhea and vomiting, hypothyroidism, mechanical obstruction of urine outflow (prostate tumors), and liver damage. In the initial stage of acute glomerulonephritis, the SCF decreases not only due to impaired glomerular membrane permeability, but also as a result of hemodynamic disorders. In chronic glomerulonephritis, the SCF decreases due to azotemic vomiting and diarrhea.

A persistent drop in SCF to 40 ml/min in chronic renal pathology indicates severe renal failure, a drop to 15-5 ml/min indicates the development of terminal CRF.

Some drugs (e.g. cimetidine, trimethoprim) reduce tubular secretion of creatinine, facilitating an increase in its concentration in the blood serum. Cephalosporin antibiotics, due to interference, lead to falsely elevated results of creatinine concentration determination.

Laboratory criteria for stages of chronic renal failure

Stage	Phase	Blood creatinine, mmol/l	SCF, % of expected
I - latent	A	Norm	Norm
	B	Up to 0.18	Up to 50
II - azotemic	A	0.19-0.44	20-50
	B	0.45-0.71	10-20
III - uremic	A	0.72-1.24	5-10
	B	1.25 and above	Below 5

An increase in the SCF is observed in chronic glomerulonephritis with nephrotic syndrome, in the early stage of hypertension. It should be remembered that in nephrotic syndrome, the value of endogenous creatinine clearance does not always correspond to the true state of the SCF. This is due to the fact that in nephrotic syndrome, creatinine is excreted not only by the glomeruli, but is also secreted by the altered tubular epithelium, and therefore the K _of endogenous creatinine can exceed the true volume of the glomerular filtrate by up to 30%.

The endogenous creatinine clearance value is affected by the secretion of creatinine by the renal tubular cells, so its clearance may significantly exceed the true value of the SCF, especially in patients with kidney disease. To obtain accurate results, it is extremely important to collect a complete urine sample for a precisely defined period of time; incorrect urine collection will lead to false results.

In some cases, to increase the accuracy of determining endogenous creatinine clearance, H2-histamine receptor antagonists are prescribed ₍ usually cimetidine at a dose of 1200 mg 2 hours before the start of daily urine collection), which block tubular secretion of creatinine. Endogenous creatinine clearance measured after taking cimetidine is almost equal to the true SCF (even in patients with moderate and severe renal failure).

To do this, you need to know the patient's body weight (kg), age (years), and serum creatinine concentration (mg%). Initially, a straight line connects the patient's age and body weight and marks a point on line A. Then, the serum creatinine concentration is marked on the scale and connected with a straight line to a point on line A, continuing it until it intersects with the endogenous creatinine clearance scale. The point of intersection of the straight line with the endogenous creatinine clearance scale corresponds to the SCF.

Tubular reabsorption. Tubular reabsorption (TR) is calculated by the difference between glomerular filtration and minute diuresis (D) and is calculated as a percentage of glomerular filtration using the formula: TR = [(SCF-D)/SCF]×100. Normally, tubular reabsorption ranges from 95 to 99% of the glomerular filtrate.

Tubular reabsorption may vary significantly under physiological conditions, decreasing to 90% with water load. A marked decrease in reabsorption occurs with forced diuresis caused by diuretics. The greatest decrease in tubular reabsorption is observed in patients with diabetes insipidus. A persistent decrease in water reabsorption below 97-95% is observed with primary and secondary shrunken kidney and chronic pyelonephritis. Water reabsorption may also decrease in acute pyelonephritis. In pyelonephritis, reabsorption decreases earlier than the decrease in SCF. In glomerulonephritis, reabsorption decreases later than SCF. Usually, simultaneously with a decrease in water reabsorption, insufficiency of the concentrating function of the kidneys is detected. In this regard, a decrease in water reabsorption in the functional diagnostics of the kidneys is not of great clinical importance.

Increased tubular reabsorption is possible in nephritis and nephrotic syndrome.