Lithium nephropathy

Introduction to lithium kidney disease Lithium nephropathy is a kidney damage caused by a lithium preparation. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: acute renal failure

Cause of lithium kidney disease

Renal water metabolism dysfunction (25%):

It is currently believed that lithium may cause polyuria and polydipsia. There may be multiple mechanisms, among which the mechanism that plays a major role is a renal diabetes insipidus, which occurs in the distal part of the distal convoluted tubule and the collecting duct. The damage is characterized by impaired sensitivity to endogenous and exogenous vasopressin. Part of the mechanism by which this damage occurs is that lithium inhibits adenylate cyclase and impairs the production of cAMP by vasopressin. However, impaired production of cAMP may not be the only mechanism of this toxic effect. In addition, studies conducted in rats have shown that lithium does not alter the responsiveness of ex vivo perfused papillae to vasopressin and suggests a large response to lithium treatment. There is a factor in the plasma of the mouse that interferes with the action of vasopressin at the receptor site of the distal nephron.

In patients with polyuria and polydipsia treated with lithium preparations, the production of electrolyte-free water during water load is not damaged, but its ability to reabsorb solute-free water in the absence of water is significantly reduced, taking thiazide diuretic Both of the above symptoms can be alleviated after the drug, and the thiazide diuretic can produce an antidiuretic effect by reducing the delivery of water to the distal nephron during renal collapse. This effect is achieved by diuretic diuretic and reducing cells. External capacity, reduced glomerular filtration rate and increased fraction of proximal tubule sodium and water reabsorption, thiazide diuretics also increase lithium reabsorption, may cause rapid lithium excretion, potassium-sparing diuretic Amiloride Lithium-induced polyuria can be alleviated by inhibiting lithium uptake by distal tubule cells.

Uric acid dysfunction (20%):

In addition to impaired urinary concentration, severe cases may have urinary dysfunction in the distal part. Perez et al reported that most of the cases have this disorder, but Donker et al found only 2 in acid in 28 individuals taking lithium. Uric acidification after loading could not reach pH 5.4, and Coppen et al. did not find uric acid dysfunction in 16 individuals who took lithium for 1 to 12.5 years, respectively.

The study found that as long as the plasma bicarbonate level is normal, the bicarbonate excretion fraction is small, and the urinary phosphorus and ammonia excretion fractions are normal, suggesting that lithium-induced urinary acidosis occurs in the distal rather than the proximal tubule.

Acute renal failure (20%):

Acute lithium toxicity in humans and animals can lead to acute renal failure, the mechanism involves tubule cell degeneration and necrosis. Evan and Ollerich have studied the ultrastructural changes of the disease, found that mitochondrial swelling, rough endoplasmic reticulum expansion and apical cells The quality is swollen, and there is renal tubular necrosis in human acute renal failure caused by lithium poisoning.

At present, most scholars' studies have not suggested that the course of treatment with lithium is significantly related to the degree of functional impairment. Renal biopsy has been performed on 7 patients with acute renal failure who have undergone renal biopsy. The results show that the main changes are interstitial fibrosis and Focal tubular atrophy, these pathological changes are clearly not associated with acute renal failure, and another renal biopsy study, while a group of patients with acute renal failure associated with acute lithium poisoning and a group of lithium without acute toxicity In the treatment of patients, it was found that pathological changes such as interstitial leukocyte infiltration, tubule dilatation and degeneration associated with acute toxicity were not significantly different between the two groups, and acute ischemic tubular necrosis was not acute in acute renal failure. Seen in patients with lithium poisoning.

Lithium kidney disease prevention

Mainly in the treatment of mental illness, we must carefully use lithium drugs and other related drugs that may cause this disease. For patients with obvious symptoms of lithium poisoning, they should be actively symptomatic to prevent more serious interstitial nephritis and kidney damage.

Lithium kidney disease complications Complications acute renal failure

Mainly complicated by acute renal failure.

Symptoms of lithium nephropathy Common symptoms Responsive dullness Diabetes dysfunction disorder Proteinuria tremor Polyuria ataxia Disorder Neuromuscular symptoms Coma

Acute lithium poisoning can present with mental and neuromuscular symptoms, including apathy, unresponsiveness, tremors, rigidity and ataxia, and conscious disturbances and coma.

Acute lithium poisoning can lead to acute renal failure and a variety of renal diseases, including chronic tubulointerstitial disease, renal diabetes insipidus and concentrating dysfunction, incomplete distal tubulic acidosis, progressive tubulointerstitial disease, distal tubules Microcapsule formation, acute renal failure, ADH resistance urinary concentrating dysfunction, but reversible, more common in more than 50% of patients with long-term lithium treatment, about 20% of cases can have polyuria, 85% of long-term lithium treatment GFR was normal, 15% had mild GFR damage, and significant GFR decline was only seen in patients who received lithium for more than 10 to 15 years.

In the literature, there was a case of chronic lithium poisoning. The proteinuria had reached the range of nephropathy. The nephrotic proteinuria disappeared after the lithium preparation was stopped. The patient did not find other causes to explain the nephrotic proteinuria. The patient developed a range of nephrotic diseases. Whether proteinuria is related to lithium poisoning cannot be denied.

Examination of lithium kidney disease

1. Urine examination of mild proteinuria, 24h urine protein quantification <2g, mainly low molecular proteinuria, urine routine examination may have white blood cells, aseptic pyuria, sometimes visible microscopic hematuria or gross hematuria, urine sugar can be Positive.

2. Renal tubular function test urine concentration dilution test function is poor, urine amino acid, bicarbonate increased, uric acid can not reach pH 5.4, urine pH> 6, urine titratable acid reduction, urine N-acetyl--D- Glucosidase (NAG) concentration increases, patients with acute renal failure may have urea nitrogen, creatinine increased.

3. Renal biopsy in patients with acute renal failure associated with acute renal failure and lithium-treated patients without acute toxicity, renal biopsy can be seen with acute toxicity associated with interstitial leukocyte infiltration, tubular dilatation and degeneration and other pathological changes, long-term acceptance of lithium Interstitial fibrosis and focal tubule atrophy were observed in the treated patients. Renal biopsy showed that the disease had characteristic pathological changes in the distal renal tubules and collecting ducts. Under the light microscope, cell swelling related to PAS-positive glycogen accumulation was observed. And vacuolization, this lesion exists in all patients with lithium-treated biopsy, appeared several days after the start of lithium treatment, disappeared after stopping lithium treatment, this characteristic lesion can also be seen in the kidney of lithium poisoned rabbit, but in Rats with glycogen-free tubular cells did not have the characteristic acute glycogen accumulation in the distal tubules and collecting ducts during lithium poisoning.

4. Imaging examination The early performance of urinary tract X-ray examination is not obvious. The typical manifestation of renal papillary necrosis in the late stage shows that the shape of the kidney is changed in the plain plain film.

Diagnosis and diagnosis of lithium kidney disease

Diagnostic criteria

According to clinical manifestations, laboratory tests, renal biopsy and long-term history of lithium treatment, the disease can be diagnosed. Generally, after receiving lithium preparations, polyuria and polydipsia and neuromuscular symptoms, such as apathy and unresponsiveness, may occur. Patients with tremors, rigidity and ataxia, and even those with disturbances of consciousness and coma should consider lithium poisoning, such as acute renal failure associated with acute lithium poisoning and various renal diseases, including chronic tubulointerstitial disease. ADH-resistant urinary concentrating dysfunction occurs, and GFR is normal or mildly impaired by GFR (a significant reduction in GFR may occur in patients receiving lithium for more than 10 to 15 years). This disease can be diagnosed at this time.

Differential diagnosis

Pay attention to the differentiation of other diseases such as polyuria and polydipsia caused by chronic interstitial nephritis and renal diabetes.

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