Chronic lead poisoning is a systemic disease mainly of the nervous, digestive and hematopoietic systems caused by exposure to lead fumes or lead dust. 1 Morphological changes of the kidney 1.1 Naked eye morphology of the kidney
We observed the kidneys of two cases of lead nephropathy with ultrasound, and found that one case had slightly enhanced echogenicity, one case had no obvious abnormality, and the volume of the two cases was within the normal range. Regarding the changes of kidney volume after the kidney damage of lead poisoning, it was reported abroad that the kidney volume was reduced in 47 out of 53 patients who died from chronic lead nephropathy. 1.2 Pathological morphology of kidney The early pathological morphological changes of kidney are mainly in the proximal tubule, and in the late stage, glomerular swelling, glomerular adhesion, local fibrosis in the interstitium, tubular atrophy and inflammatory cell infiltration are seen. Animal experiments found that the damage of lead on kidney can be divided into three stages: Early stage: the exposure time of lead is shorter than 1 year, and the epithelial cells of proximal tubule are seen to have intranuclear inclusion bodies. The urinary lead pencil is increased, while the kidney function is normal. The alteration of its sub-microstructure is reversible. Intermediate stage: with lead exposure longer than 1 year, the ability of the epithelial cells of the proximal tubule to form intranuclear inclusion bodies is reduced. There is a moderate amount of fibrous tissue proliferation in the renal interstitium. Urinary lead excretion is reduced. Clinical examination of renal function is still within normal limits. The lesions that have developed are generally not easily recovered. Late stage: Longer periods of lead exposure cause more pronounced interstitial fibrosis, resulting in interstitial nephritis and renal atrophy. Glomerular filtration rate is significantly reduced, eventually leading to chronic renal failure. 2 Alteration of effect markers 2.1 Urine protein
Chronic lead poisoning kidney damage, increased urine protein is an important effect marker, the main target site in the renal tubules, so the determination of low molecular protein urine should be the focus of work, observe the content of urine protein and the duration of the increase, can determine the degree of kidney damage, usually low molecular weight protein such as β-MG as an indicator of early damage to the renal tubules, if a large amount of β-MG can indicate that the renal tubular re However, the specificity of the diagnosis of lead nephropathy is poor. It has been proposed that α
1-MG is proposed to be better than β-MG as an indicator of early effect of lead nephropathy. 2.2 Urinary sugar After chronic lead poisoning, renal tubular reabsorption of sugar is impaired, but most of the urinary sugar is normal in the early stage. 2.3 Endogenous creatinine clearance Endogenous creatinine clearance (Ccr) can effectively reflect early renal damage, and some studies suggest that low level of lead exposure is significantly associated with reduced endogenous creatinine clearance (Ccr). 2.4 Urease
Renal tubular cells are rich in enzymes, which normally appear in the urine with cell renewal and constitute a major component of the enzyme profile, and when kidney damage occurs, the enzymes in the urine are increased; therefore, it can be used as a biomarker in kidney damage. δ-amino-γ-ketovaleric acid dehydratase (ALAD) is a key enzyme involved in heme biosynthesis and can catalyze the polymerization of two molecules of δ-amino-γ-ketovaleric acid into porphobilinogen.
ALAD is the most sensitive indicator of the response to low levels of lead exposure and an accurate indicator of lead overload in patients with advanced renal impairment. In conclusion, the manifestation of early or acute nephrotoxicity of lead is mild and limited to renal tubular epithelial cells, and the damage is reversible. If lead nephropathy is diagnosed early, lead expulsion treatment can expel inclusion bodies, restore the altered mitochondrial morphology and function, and normalize renal tubular function.