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PubMed1994

Calciuria and aminoaciduria in very low birth weight infants fed a high-mineral premature formula with varying levels of protein.

To assess the influence of protein intake on renal excretion of calcium and amino acids and on bone mineralization in preterm infants, we randomly selected within weight group strata 27 infants who weighed < 1500 gm at birth (nine per group) to be fed a high-mineral (calcium, 940 mg/L; phosphorus, 470 mg/L) premature formula with one of the following protein contents: formula A, 3.0 gm/100 kcal; formula B, 2.7 gm/100 kcal; and formula C, 2.2 gm/100 kcal. Mean (+/- SD) daily weight gain was greater in infants receiving the higher protein intakes for the first 30 days (formula A, 24.8 +/- 5.1 gm; formula B, 20.5 +/- 3.8 gm; formula C, 16.2 +/- 5.9 gm (analysis of variance: p < 0.01; C < A, p < 0.05)). Bone mineral content did not differ at any time point, and all groups had a high prevalence of generalized aminoaciduria (4 weeks: formula A, 56%; formula B, 71%; formula C, 75%). Urinary calcium corrected for creatinine (in milligrams per milligram) increased as protein content decreased (2 weeks: formula A, 0.16 +/- 0.10; formula B, 0.20 +/- 013; formula C, 0.44 +/- 0.33 (C > A, C > B, p < 0.05); 4 weeks: formula A, 0.23 +/- 0.15; formula B,0.34 +/- 0.47; formula C, 0.49 +/- 0.22 (C > A, p < 0.01). We conclude that the high mineral content and other components of premature formulas result in a higher growth rate and may increase protein requirements. Failure to meet protein requirements may result in underutilization of absorbed calcium and increased renal excretion of calcium. In preterm infants, higher protein intake probably supports rather than jeopardizes bone mineral accretion, and reduces rather then increases calciuria.

Acetylglucosaminidase↗
PubMed1978

Proximal tubulare dysfunction associated with Burkitt's lymphoma.

Generalized aminoaciduria, uricosuria, glycosuria and phosphaturia were discovered in a patient with advanced Burkitt's lymphoma with renal infiltration. The literature is reviewed and three pathogenetic mechanisms are discussed. It is presumed that proximal tubular dysfunction in this case was related to the marked peritubular infiltrate causing cell mediated immunological injury or direct tubular destruction by tumor.

Adult↗
PubMed1985

Impaired potassium and magnesium homeostasis in acute tubulo-interstitial nephritis.

Although acute tubulo-interstitial nephritis is increasingly recognized as a cause of acute renal failure, little is known about renal tubular function in this disease. We report on two patients with acute tubulo-interstitial nephritis who demonstrated abnormalities in proximal and distal tubular function. The first patient developed hyperkalemia presumably from a potassium secretory defect in the distal nephron. The second patient developed an incomplete Fanconi's syndrome with glycosuria and aminoaciduria and two heretofore unreported complications of acute interstitial nephritis: hypokalemia and hypomagnesemia secondary to urinary losses of these cations. Careful monitoring of renal tubular function is indicated in patients with acute tubulo-interstitial nephritis.

Acute Disease↗
PubMed1987

Tumor-induced osteomalacia: long-term follow-up of two patients cured by removal of their tumors.

Two patients with mesenchymal tumors had osteomalacia associated with marked hypophosphatemia and renal phosphate wasting. Their serum calcium and parathyroid hormone levels were normal. The first patient also had aminoaciduria and glucosuria in addition to phosphaturia. Both patients were treated with very large doses of vitamin D2 and phosphate without improvement in the osteomalacia or normalization of the serum phosphate. Complete removal of a low-grade fibrosarcoma in the second patient and removal of an ossifying fibroma in the first patient resulted in a cure in both patients despite no further therapy with vitamin D or phosphate. The excessive aminoaciduria and glucosuria of the first patient also remitted. During a 14-year follow-up period, there has been no evidence of tumor recurrence, hypophosphatemia, or osteomalacia in either patient. The levels of 1,25-dihydroxycholecalciferol remain within the normal range in both patients.

Adult↗
PubMedDate not supplied

Hypophosphataemic osteomalacia due to de Toni-Debre-Fanconi syndrome in a 19-year old girl.

Osteomalacia associated with adult onset Fanconi syndrome is thought to result from hypophosphataemia due to renal phosphate loss and relative 1,25-dihydroxyvitamin D3 deficiency. In this disorder, the impaired renal phosphate uptake occurs as part of a generalized tubular defect in association with other features such as bicarbonuria, glycosuria and aminoaciduria. Fanconi syndrome is either hereditary--juvenile form--or is associated with various acquired or heritable diseases. In adults, the disease is similar to the juvenile form, but osteomalacia is a prominent feature. We report a sporadic, adult onset, hypophosphataemia in a 19-year old female patient who presented after puberty complaining of bone and joint pain and difficulty in walking following a minor fall. Radiological examination revealed numerous bilateral fractures of the ribs and pelvis while biochemical investigations showed combination of high phosphate clearance, low serum bicarbonate, glycosuria and glycinuria. Known causes of acquired renal tubular dysfunction were ruled out. The patient was diagnosed as having idiopathic Fanconi syndrome and started on vitamin D3 (Alfacalcidol 1 mg/day) and oral phosphorus (Joulie Solution, 1.5 g/day), which led to resolution of symptoms and an increase in serum phosphate (from 0,54 to 0,71 mmol/l) within few months following the initiation of therapy. However, radiological re-examination showed no signs of fracture healing.

Adult↗
PubMed1979

Effects of dietary cadmium on rhesus monkeys.

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.

Animals↗
PubMed1992

Clinical features of Balkan endemic nephropathy.

This paper describes the clinical symptoms and signs of Balkan endemic nephropathy (BEN). The initial asymptomatic period followed by weakness and lassitude during renal insufficiency is emphasized. Non-characteristic lumbar pain may be present and episodes of macrohaematuria may occur. There is no fever, no severe dysuria, and no general disease preceding the symptoms. No oedema of the nephrotic type is recognized. Working capacity is unaffected until the late stage of the disease. In the advanced stages pallor of the skin and xantochromia of palms and soles are noticeable. Blood pressure is normal, but in the advanced phase may be elevated. In the uraemic phase a full uraemic syndrome is found. Urothelial tumours are frequent, occurring in 2-47% of cases; tumour cells may be found in the urine. Proteinuria of tubular type may be found early; in the uraemic phase it is constant. In the urinary sediment there are scarce white and red blood cells (the latter episodically abundant). Bacteriuria is present in about 20% of women patients. Glucosuria (less than 10%) and aminoaciduria (less than 10%) have been reported. In the early stages of BEN the urine concentration capacity is impaired earlier than renal blood flow and glomerular filtration rate. Enzymuria is present in the early phases. Tamm-Horsfall protein may be increased in the urine. Normo- or hypochromic normocytic hyporegenerative anaemia is a frequent finding. Bone marrow and leucocytes are normal. Serum proteins and immunoglobulins are not altered. Complement is normal; anti-glomerular basal membrane and anti-tubular basal membrane are negative. On radiography, kidney size varies from normal to the size of a small contracted kidney. The clinical picture of the disease is that of a slowly progressing tubulo-interstitial chronic nephritis.

Balkan Nephropathy↗
PubMed1993

Renal tubular dysfunction in chronic alcohol abuse--effects of abstinence.

BACKGROUND: Alcohol abuse may be accompanied by a variety of disorders of electrolyte and acid-base metabolism. The role of the kidney in the pathogenesis of these disturbances is obscure. We sought to evaluate the alcohol-induced abnormalities of renal function and improvement during abstinence and to assess the relation between renal dysfunction and electrolyte and acid-base disorders. METHODS: We measured biochemical constituents of blood and renal function before and after four weeks of abstinence in 61 patients with chronic alcoholism who had little or no liver disease. RESULTS: On admission, 18 patients (30 percent) had hypophosphatemia and hypomagnesemia, 13 patients (21 percent) had hypocalcemia, and 8 patients (13 percent) had hypokalemia. Twenty-two patients (36 percent) had a variety of simple and mixed acid-base disorders. Twenty of these patients had metabolic acidosis, and among them, 80 percent had alcoholic acidosis. A wide range of defects in renal tubular function, with normal glomerular filtration rate, were detected in these patients. The defects included decreases in the threshold and maximal reabsorptive ability for glucose (38 percent of patients) and in the renal threshold for phosphate excretion (36 percent); increases in the fractional excretion of beta 2-microglobulin (38 percent), uric acid (12 percent), calcium (23 percent), and magnesium (21 percent); and aminoaciduria (38 percent). Seventeen patients (28 percent) had a defect in tubular acidification, and five an impairment in urinary concentrating ability. Urinary excretion of N-acetyl-beta-D-glucosaminidase and alanine aminopeptidase were increased in 41 and 34 percent of patients, respectively. The abnormalities of blood chemistry and renal tubular function disappeared after four weeks of abstinence. CONCLUSIONS: Transient defects in renal tubular function are common in patients with chronic alcoholism and may contribute to their abnormalities of serum electrolyte and blood acid-base profiles.

Acid-Base Imbalance↗
PubMed2006

[Acquired Fanconi-de Toni-Debre syndrome due to therapy for Ewing's sarcoma in 5-years old boy].

We present a 5-years old boy with acquired Fanconi-de Toni-Debre syndrome being a effect of therapy for Ewing's sarcoma. At the age of 3 years, this boy was diagnosed as suffering from Ewing sarcoma of his right femur. The boy received a course of 8-month pre-surgery (6 VIDE--Vincristine, Ifosfamide, Doxorubicin, Etoposide cycles and 2 VAI--Vincristine, Actinomycin, Ifosfamide cycles) and 6-month post-surgery (6 VAI--Vincristine, Actinomycin, Ifosfamide cycles) cytostatic therapies according to EWING, EURO 99 protocol. In forth month of post-surgery cytostatic therapy, progressive malaise, polyuria, polydypsia, and recurrent vomiting occurred. The association between those symptoms and malignancy was excluded. Laboratory studies revealed hypokaliemia, hypophosphatemia, proximal tubular acidosis, proteinuria, glucosuria, aminoaciduria, hyperkaliuria and hyperphosphaturia. Acquired Fanconi-de Toni-Debre syndrome due to toxic effect of cytostatic therapy on renal proximal tubules was diagnosed. At present, two years after the time the diagnosis was made, despite constant substitution of potassium, phosphates and bicarbonates, deficit of body mass and height, and bone mineral density abnormalities are observed.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Renal function in children and adolescents following 72 g/m2 of ifosfamide.

A detailed analysis of the renal function of 18 children and adolescents aged 7-20 years (median, 16 years) was performed at least 3 months following the completion of a non-platinum-containing chemotherapy regimen with a total dose of 72 g/m2 of ifosfamide. Ifosfamide had been given as a 1-h infusion of 1.8 g/m2 daily for 5 days at 5- to 6-week intervals along with mesna uroprotection. The mean glomerular filtration rate (GFR) as determined by inulin clearance was 100 ml/min/1.73 m2. Although 6 of 18 patients had GFRs below normal, the lowest was only 18% less than the lower limit of normal and would not account for any clinical compromise. The renal plasma flow and filtration fraction were normal. Proximal tubular function evaluation revealed normal fractional excretion (FE) of glucose; normal mean tubular maximum phosphate reabsorption per GFR (TMP)/GFR values; high FE of urate (17%); and mild, generalized aminoaciduria in 6 of the 18 patients. Distal tubular function evaluation showed normal 24-h urinary calcium levels and FE of magnesium as well as normal urinary osmolality after water deprivation. Two patients had mild proteinuria. The findings in this study are encouraging in terms of the lack of clinically significant renal abnormalities observed in patients who had received a cumulative dose of 72 g/m2 of ifosfamide.

Adolescent↗
PubMed1984

Proximal renal tubular dysfunction in severe burns.

Proximal renal tubular function was studied in 11 patients with severe burn injury. Creatinine clearance was normal or increased in ten patients. Fractional excretion of sodium was less than 1% in ten. Fractional excretion of uric acid and amylase were increased in all but four and two cases, respectively, while absolute clearances of lysozyme and beta 2-microglobulin were increased in all but one patient. Renal threshold phosphate concentration was reduced in four patients. Twenty-four-hour urine glucose excretion exceeded 1 g in five patients, aminoaciduria was noted in eight, and proteinuria, predominantly globulinuria, was present consistently. Metabolic acidosis was seen in one patient, and transient hypokalemia occurred in two. Abnormalities of proximal tubular function were more marked in the five patients with the greatest extent of third-degree burns who died. The cause of proximal tubular dysfunction is not clear and may be related to an adaptive response to severe injury.

Adult↗
PubMed2006

Heterogeneous mutations in the SLC3A1 and SLC7A9 genes in Chinese patients with cystinuria.

Cystinuria is a recessively inherited aminoaciduria that leads to recurrent urolithiasis. It is caused by the defective transport of cystine and dibasic amino acids in the proximal renal tubules and intestinal epithelium. Two genes responsible for this, SLC3A1 and SLC7A9, are known. Patients with two SLC3A1 mutations are classified as type A cystinuria, whereas patients with two SLC7A9 mutations are classified as type B cystinuria. Few clinical and molecular data have been reported for Asian cystinuria patients. In this study, we determined the molecular basis of cystinuria in eight unrelated Chinese subjects. Coding exons and flanking introns of the SLC3A1 and SLC7A9 genes were directly sequenced after amplification by polymerase chain reaction. Five different SLC3A1 mutations were found. Two missense mutations, D210G and S547L, were novel. The other three SLC3A1 mutations (IVS6+2T>C, R181Q and R365W) have been described previously. In addition, four novel SLC7A9 mutations, C137R, c.730delG, IVS10+2_3delTG and IVS12+3insT, together with two previously reported mutations (A70V and G195R) were found. All patients except one carried compound heterozygous mutations. IVS12+3insT was detected in patients from two families. This is the first molecular genetic study on Chinese cystinuria patients. Three patients with type A cystinuria, two with type B cystinuria, and three carriers of type B cystinuria were identified. Our results suggest that the molecular basis of cystinuria is heterogeneous in our local population.

Adult↗
PubMed1979

Renal tubular dysfunction in transplanted kidneys.

We studied 15 renal transplant recipients for evidence of tubular dysfunction. Eight patients were hypophosphatemic, and two had systemic acidosis with a urinary acidification defect. Mild aminoaciduria and bicarbonaturia were present in four and 14 patients, respectively. Elevated parathyroid hormone level was found in only one patient. Tubular reabsorption of phosphorus was depressed in all eight hypophosphatemic patients, while no such abnormalities were observed in 14 control subjects. Defective tubular reabsorption of phosphorus was the most striking abnormality. None of the parameters studied, including immunosuppressant therapy, parathyroid hormone levels, creatinine clearance, or acid-base balance, clearly account for the pathogenesis of this abnormality.

Acidosis↗
PubMed2000

[Peritoneal dialysis in children after cardiac surgery].

The authors analyse their experience with the use of peritoneal dialysis (PD) in children with acute renal failure after cardiac surgery. From 1995 through 1998, 1246 children were operated in Pediatric Cardiocenter 38 of them developed acute renal failure and required peritoneal dialysis. Indications for PD were oliguria, anuria, hyperkalemia and fluid overload with generalized tissue oedema. PD was instituted at mean 33.9 (3-132) hours after surgery and lasted mean 53.7 (6-264) hours. None of the patients developed peritoneal infection. Hyperglycaemia developed in 8 patients and was treated with continuous insulin infusion. 5 patients required catheter reposition or reinsertion due to inadequate fluid removal and 1 patient required another renal replacement therapy. 22 (57.9%) patients died due to intractable low cardiac output. 16 survivors recovered their renal functions. In a long-term follow-up, 7 patients had no signs of significant renal dysfunction. In 4 patients, mild elevation of N-acetyl-beta-D-glukozaminidase indicates mild proximal tubular dysfunction. These findings together with aminoaciduria in 5 patients will require a further follow-up. (Tab. 2, Fig. 1, Ref. 16.)

Acute Kidney Injury↗
PubMed2002

Cd-MT causes endocytosis of brush-border transporters in rat renal proximal tubules.

Nephrotoxicity in humans and experimental animals due to chronic exposure to cadmium (Cd) is manifested by defects in the reabsorptive and secretory functions of proximal tubules (PT). The main symptoms of Cd nephrotoxicity, including polyuria, phosphaturia, aminoaciduria, glucosuria, and proteinuria, suggest that various brush-border membrane (BBM) transporters are the main targets of Cd. Specific transporters may be either directly inhibited by Cd or lost from the BBM after Cd treatment, or both. We have recently proposed that Cd may impair the vesicle-dependent recycling of BBM transporters by inhibiting vacuolar H+-ATPase (V-ATPase) activity and endocytosis in PT cells (Herak-Kramberger CM, Sabolic I, and Brown D. Kidney Int 53: 1713-1726, 1998). The mechanism underlying the Cd effect was further explored in an in vivo model of experimental Cd nephrotoxicity induced by Cd-metallothionein (Cd-MT; 0.4 mg Cd/kg body mass; a single dose sc) in rats. The time-dependent redistribution of various BBM transporters was examined in this model by fluorescence and gold-labeling immunocytochemistry on tissue sections and by immunoblotting of isolated renal cortical BBM. In PT cells of Cd-MT-treated rats, we observed 1) shortening and loss of microvilli; 2) time-dependent loss of megalin, V-ATPase, aquaporin-1 (AQP1), and type 3 Na+/H+ exchanger (NHE3) from the BBM; 3) redistribution of these transporters into vesicles that were randomly scattered throughout the cell cytoplasm; and 4) redistribution of NHE3, but not megalin, into the basolateral plasma membrane. The internalization of BBM transporters was accompanied by fragmentation and loss of microtubules and by an increased abundance of alpha-tubulin monomers in PT cells. Transporter redistribution was detectable as early as 1 h after Cd-MT treatment and increased in magnitude over the next 12 h. We conclude that the early mechanism of Cd toxicity in PT cells may include a colchicine-like depolymerization of microtubules and impaired vesicle-dependent recycling of various BBM proteins. These processes may lead to a time-dependent loss of cell membrane components, resulting in reabsorptive and secretory defects that occur in Cd-induced nephrotoxicity.

Animals↗
PubMed1991

Clinical and laboratory findings in the oculocerebrorenal syndrome of Lowe, with special reference to growth and renal function.

BACKGROUND: The oculocerebrorenal syndrome of Lowe is an X-linked disorder whose clinical manifestations include congenital cataracts, mental retardation, and renal tubular dysfunction. We investigated growth, renal function, and serum chemistry values in patients with the oculocerebrorenal syndrome to determine the natural history of the disorder and its heterogeneity with respect to these characteristics. METHODS: Twenty-three patients with the oculocerebrorenal syndrome, ranging in age from 4 months to 31 years, were examined. Height was compared with bone age. Renal function was assessed by measurements of proteinuria, urinary volume, and fractional excretions of potassium, phosphate, carnitine, and amino acids. Creatinine clearance was determined as a measure of glomerular function. RESULTS: In the oculocerebrorenal syndrome, linear growth decreases after one year of age; bone age lies between chronologic age and height age. Renal dysfunction occurs in the first year of life, characterized by proteinuria (mean [+/- SD], 1.38 +/- 0.77 g of urinary protein per square meter of body-surface area per day; normal, less than or equal to 0.10), generalized aminoaciduria (mean, 686 +/- 505 mumol of urinary amino acid per kilogram of body weight per day; normal, 94 +/- 45), carnitine wasting (mean fractional excretion, 0.10 +/- 0.05; normal, 0.03 +/- 0.01), and phosphaturia progressing into the third decade. Urinary wasting of individual amino acids is milder than in cystinosis, and branched-chain amino acids are relatively spared. Reciprocal serum creatinine levels fall linearly with age, predicting renal failure in the fourth decade. Concentrations of the muscle enzymes creatine kinase, aspartate aminotransferase, and lactate dehydrogenase, as well as of total serum protein, serum alpha 2-globulin, and high-density lipoprotein cholesterol, are elevated. CONCLUSIONS: Renal glomerular deterioration is slowly progressive in the oculocerebrorenal syndrome. Renal tubular dysfunction begins early and persists; most patients require alkalinization therapy, and many benefit from supplemental potassium, phosphate, calcium, or carnitine. Serum enzyme elevations suggest muscle involvement in the oculocerebrorenal syndrome.

Adolescent↗
PubMed1990

Ifosfamide-induced renal tubular dysfunction and rickets in children with Wilms tumor.

The renal tubular Fanconi syndrome developed in five patients with Wilms tumor after treatment with ifosfamide, a derivative of cyclophosphamide. Glomerular filtration rates were severely decreased. Renal function was investigated because of the development of rickets. All patients had undergone reduction of renal mass by nephrectomy. None had preexisting renal tubular injury. The syndrome developed at cumulative doses of ifosfamide of 39 to 99 gm/m2. Low serum bicarbonate and phosphate concentrations with glucosuria, aminoaciduria, and hypochloremic metabolic acidosis were the manifestations of the Fanconi syndrome. Bicarbonate and phosphate replacement resulted in bone healing, but recovery of tubular and glomerular function did not occur. Monitoring of these laboratory values during ifosfamide therapy could allow earlier replacement therapy to prevent severe bone disease.

Child↗
PubMedDate not supplied

Cadmium nephropathy.

Cadmium, an important environmental toxic agent has the kidney as its most important target organ. It is concentrated mainly in the renal cortex. Excessive renal accumulation of cadmium causes well defined morphological and ultrastructural pathological changes in the proximal tubules. Functional changes accompanying cadmium nephropathy include proteinuria, enzymuria, aminoaciduria, glycosuria, polyuria, hepercalciuria, increased urinary uric acid, and cadmium. The observed proteinuria has two components: low molecular weight proteinuria of tubular origin (excess excretion of proteins such as B2-microglobulin) and high molecular weight proteinuria of glomerular origin, (excretion of proteins such as albumin, IgG, transferrin, etc.) The proposed mechanisms of cadmium nephropathy are reviewed. The involvement of metallothionein in cadmium nephropathy and the nephrotoxic effects of cadmium-thionein are discussed.

Animals↗