Toxic nephropathy

Introduction

Introduction to toxic nephropathy Kidney damage caused by nephrotoxic substances is often named after the name of the nephrotoxic substance. With the development of industry, the metal and smelting industry has increased. The emergence of chemical raw materials, medicines and various pesticides has increased environmental pollution, increased the chances of people exposed to kidney poisons, and increased the incidence of toxic nephropathy. Caused by kidney damage, often manifested as acute renal failure. Acute renal failure caused by toxic nephropathy accounts for about 5 to 25%. If properly treated, kidney function can return to normal. Delayed diagnosis and treatment can cause death. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute renal failure

Cause

Causes of toxic nephropathy

Reasons for kidney damage caused by nephrotoxic substances:

1 renal blood flow is large, 1/4 to 1/5 of the systemic blood flow through the kidneys, about 1000 ~ 1200ml per minute, toxic substances with the blood into the kidneys, will lead to kidney damage.

2 Due to the countercurrent multiplication mechanism of the kidney, the concentration of nephrotoxic substances in the medulla and renal papilla is increased, so the medulla and renal papillary lesions are significant in toxic nephropathy.

3 Nephrotoxic substances are reabsorbed and excreted by renal tubular epithelial cells, so the concentration of toxic substances in renal tubular or tubular epithelial cells is increased, which can directly damage renal tubular epithelial cells.

4 The total area of the glomerular capillary endothelium far exceeds other organs in the body, so the immune complex is easy to deposit in the glomerulus and cause immune kidney damage. Mesangial hyperplasia is caused by glomerular mesangial phagocytosis and toxic removal. With the deposition of immune substances, in addition, when the nephrotoxic substance passes through three different membranes of the glomerulus, the poison or immune complex is deposited in the glomerulus.

Many substances have potential renal toxicity, common endogenous, such as high calcium, high phosphorus, high uric acid and hyperoxalic acid can cause renal interstitial - tubulosis, exogenous, such as heavy metals (lead, cadmium , mercury, gold, uranium, copper, antimony, antimony, arsenic, lithium, zinc, etc.), chemical poisons (including organic solvents, hydrocarbons, pesticides, fungicides and coal phenols, etc.), drugs, almost all drugs have kidneys Toxicity (including antibiotics, antipyretic analgesics, metal preparations, contrast agents, diuretics, Chinese herbal medicines, etc.), clinically more common nephrotoxic drugs:

1 drugs that directly damage the kidney, aminoguanidine antibiotics (such as gentamicin kanamycin, streptomycin, etc.), cephalosporin, polymyxin, vancomycin, bacitracin, zirconia, two sex B, tetracycline, dimethyl chlortetracycline, sulfonamides, gold preparations, penicillamine, edetate (EDTA); phenyletazine indomethacin, ibuprofen, phenacetin, paracetamol, salicylic acid Salt; methotrexate; contrast agent.

2 drugs for allergic renal damage are: penicillins, cephalosporins, sulfonamides, rifampicin, aminocaproic acid, furosemide, thiazide diuretics, azathioprine, allopurinol, tri-double Ketone, phenytoin, phenobarbital and the like.

3 drugs manifested as crystalline nephropathy or urinary tract obstructive nephropathy: sulfa drugs.

4 biotoxic (animal, phytotoxic), including bee venom, snake venom, raw fish gall, scorpion venom and pollen.

5 physical factors such as radiation, heat stroke, electroshock and so on.

Prevention

Toxic nephropathy prevention

1 Stop exposure to poison.

2 to promote the excretion of poisons, infusion, application of detoxification drugs, if necessary, dialysis treatment, where the molecular weight is small, less protein binding, evenly distributed in the body, can be discharged by hemodialysis, the peritoneal dialysis effect of high protein binding rate Well, plasma replacement therapy should be used with caution.

Complication

Toxic nephropathy complications Complications acute renal failure

The main complication of this disease is acute renal failure. The focus of treatment of this disease is also on the prevention and treatment of acute renal failure.

Symptom

Symptoms of toxic nephropathy Common symptoms Polyuria, polydipsia, oliguria, diabetes, urine, urinary leukocyte, urinary kidney stones, fever, rash, lymphadenopathy

The clinical manifestations of toxic nephropathy vary with the pathogenesis. Common common manifestations are:

1 renal tubular dysfunction symptom group :

Proximal tubular dysfunction manifested as Fanconi's syndrome: glucoseuria, amino aciduria, phosphate urine, and sometimes hypokalemia, found in some heavy metal toxic nephropathy, expired tetracycline toxic nephropathy; distal renal tubular function Decreased as renal diabetes insipidus: polydipsia, polydipsia, polyuria, toxic nephropathy caused by lithium, fluoride, and methionine; renal tubular acidosis: high chloride acidosis, imbalance of water and electrolyte balance (such as hypokalemia or hyperkalemia, low sodium, hypocalcemia, polyuria, polydipsia, polydipsia, etc.); renal osteodystrophy: renal rickets or osteomalacia, renal calcification or kidney stones, etc. Toxic nephropathy caused by tyrosin B.

2 acute renal failure syndrome :

Light, only trace urine protein, red, white blood cell urine and tubular urine, oliguria or anuria-free azotemia, severe cases of typical acute renal failure syndrome, seen in aminoguanidine antibiotics, inorganic mercury Caused by toxic kidney disease.

3 acute allergic interstitial nephritis :

Fever, rash, swollen lymph nodes, joint pain, blood eosinophilia and other systemic allergies, urinary eosinophilia, a large number of proteinuria nephrotic syndrome, or hematuria, severe acute renal failure Found in various drugs, especially penicillin, sulfa drugs, anti-tuberculosis drugs and other poisoning.

4 chronic renal failure syndrome :

The clinical manifestations are similar to toxic nephropathy caused by other causes. Sometimes the renal function continues to slowly deteriorate after stopping the exposure to poison, which is seen in chronic lead poisoning nephropathy.

5 nephritis and nephrotic syndrome :

Exogenous toxins, such as penicillamine, gold salts, snake venom, bee venom, pollen, etc., cause glomerular disease, manifested as nephritic syndrome or nephrotic syndrome, these manifestations are difficult to cause small kidneys caused by other causes The ball disease is different. The patient should be asked in detail whether there is a history of renal toxic contact, which provides a basis for differential diagnosis, otherwise it is easy to be misdiagnosed and missed.

Examine

Examination of toxic nephropathy

For patients with suspected nephropathy, blood routine, urine routine, kidney B ultrasound, renal pelvic venography, renal scan, renal biopsy (electron microscopy report), urine test, renal function test, etc. should be performed.

Diagnosis

Diagnosis and diagnosis of toxic nephropathy

diagnosis

Diagnosis can be based on medical history, clinical symptoms, and laboratory findings.

Clinical diagnosis of toxic nephropathy is generally based on the history of renal toxic exposure, renal tubular and / or glomerular damage, the clinical manifestations of the toxic poisoning, by ordinary and / or special examination, clinical observation, can be caused by other causes Kidney damage. A diagnosis can be made.

Differential diagnosis

In the diagnosis of toxic nephropathy, attention should also be paid to the mild toxic nephropathy should be distinguished from the urinary tract infection. In addition to the symptoms and signs, the bacteria in the urine often have an important role in the infection.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.

Was this article helpful? Thanks for the feedback. Thanks for the feedback.