Captopril kidney damage

Introduction to Captopril Kidney Damage Renal damage caused by angiotensin inhibitor (ACEI) refers to acute interstitial nephritis, nephrotic syndrome and renal dysfunction caused by the use of a conversion enzyme inhibitor. ACEI is safe, effective and can be used by most patients. Tolerated, but some patients have some potential factors affecting renal function, such as renal artery stenosis, renal artery thrombosis, isolated kidney, transplanted kidney, etc., acute renal failure, renal tubulointerstitial can occur after the use of ACEI Lesions and other damage. basic knowledge The proportion of illness: the incidence rate is about 0.004% - 0.006% Susceptible people: no special people Mode of infection: non-infectious Complications: urinary retention

Causes of renal damage to captopril

(1) Causes of the disease

The cause of renal damage caused by ACEI is related to the clinician's failure to strictly control the indications for medication. Renal artery stenosis, renal artery thrombosis, isolated kidney and excessive use of ACEI are likely to increase the risk of kidney damage.

(two) pathogenesis

The pathogenesis of renal damage caused by ACEI may have the following aspects:

1. Hemodynamic changes: Intrarenal angiotensin II can affect renal vascular tone, causing contraction of the ball and the small arteries, resulting in reduced renal blood flow, ensuring circulating blood volume and maintaining blood pressure, and ACEI blocking blood vessels. The formation of angiotensin II reduces its effect. Compared with the small arteries of the ball, the resistance of the small arterioles decreases more obviously, which reduces the blood flow of the glomerulus, leading to a decrease in glomerular filtration rate and renal function. Damage, when the renal artery is narrow, the glomerular blood flow is reduced, and the glomerular filtration rate is maintained by the contraction of the small arterioles. When the ACEI is used, the small arterioles are dilated and the glomerulus is filtered. The rate drops sharply, causing acute renal failure.

2. Direct toxic effects of ACEI on proximal convoluted epithelial cells: may be related to the blocking of the function of certain key esterases in proximal convoluted epithelial cells by ACEI, or ACEI may hinder the recovery of cells after ischemia, aggravating ischemia Reperfusion of cellular damage, resulting in acute tubular necrosis.

3. Allergic factors and immune regulation disorders: may be related to the release of renal interstitial monocytes, lymphocyte infiltration and the release of certain cytokines (such as interleukin-1, interleukin-2, tumor necrosis factor-) .

Captopril prevention of kidney damage

1. Strict control of medication indications: Before the medication, there are clear risk factors such as renal artery stenosis, hypertensive nephrosclerosis, renal artery thrombosis, especially severe bilateral renal artery stenosis and isolated kidney, if any ACEI should be used with caution or disabled.

2. Pay attention to observe the timely withdrawal of drugs: In the first week of using ACEI, renal function should be strictly detected and urine routine and blood potassium should be checked. Once renal dysfunction is found, the drug should be stopped in time, and renal function should be reviewed in a short period of time. After that, it can be fully recovered.

3. Active treatment of acute renal failure.

Complications of gallstones and renal damage Complications, urinary retention

Hyperkalemia and urinary sodium retention.

Hyperthyroidism Syndrome No urinary renal artery stenosis Renal glucosuria Renal failure Renal urinary kidney damage

Kidney performance

(1) Acute renal failure: mild manifestations of renal dysfunction found by chance, asymptomatic increase in serum creatinine, increased by >100 mol/L, decreased endogenous creatinine clearance, decreased glomerular filtration rate 50%, in patients with renal artery stenosis, especially bilateral renal artery stenosis, sudden oliguria or anuria, rapid deterioration of renal function in a short period of time, can be manifested as acute renal failure.

(2) acute interstitial nephritis: clinical manifestations of proteinuria, generally less than 2g / 24h, renal glucosuria, rash and blood eosinophilia.

(3) nephrotic syndrome: manifested as a large amount of proteinuria, hypoalbuminemia, with or without hyperlipidemia and edema, may have hypertension, renal biopsy is membranous nephropathy.

2. Extrarenal performance: may have cough, high blood potassium, elevated urine and so on.

Examination of renal damage of captopril

Routine hematuria test: visible proteinuria, diabetes, increased urinary sodium, blood urea nitrogen, elevated creatinine, decreased endogenous creatinine clearance, decreased glomerular filtration rate, eosinophilia.

Histopathological examination: degeneration and necrosis of renal tubular epithelial cells were observed under light microscopy. The infiltration of renal interstitial cells was mononuclear, lymphocytes, neutrophils and eosinophils infiltration, and some patients had small ball lesions. Most of them showed membranous nephropathy. Immunofluorescence showed IgG, IgM and C3 deposition. Under electron microscope, there was spherical electron dense deposit in glomerular capillary basement epithelial cells.

Diagnosis and diagnosis of renal damage caused by captopril

diagnosis

The diagnosis of this disease should have the following conditions:

1. Clinical application of ACEI history.

2. Short-term renal dysfunction, increased proteinuria or proteinuria, renal glucosuria, increased urinary sodium.

3. Sudden occurrence of oliguria or anuria, rapid deterioration of renal function in the short term, manifested as acute renal failure, acute interstitial nephritis or nephrotic syndrome should be suspected of this disease.

Differential diagnosis

1. Primary membranous nephropathy: The disease occurs in men over 40 years old. It is more common in nephrotic syndrome. Before using ACEI, it is necessary to rule out the presence of potential membranous nephropathy and identify it according to the reaction after stopping the drug. Those caused by ACEI can relieve themselves after stopping the drug.

2. Rapidly progressive nephritis: The system has severe systemic symptoms, with severe oliguria and no urine, and rapidly develops into uremia. The urine test shows a lot of red blood cells or gross hematuria, a small amount or a moderate amount of proteinuria, and the urine specific gravity is generally not Low, more than 50% of the renal biopsy has a crescent formation, which can be identified.

3. Kidney damage caused by aminoglycoside antibiotics: Patients with this disease have a history of applying aminoglycosides, proteinuria, hematuria, tubular urine, renal dysfunction after 5 to 7 days of treatment, renal glomeruli at renal biopsy Epithelial cell degeneration, vacuolization and necrosis, interstitial cell infiltration, glomerular substantially normal.

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