Renal effects of environmental and occupational lead exposure

Environmental and industrial lead exposures continue to pose major public health problems in children and in adults. Acute exposure to high concentrations of lead can result in proximal tubular damage with characteristic histologic features and manifested by glycosuria and aminoaciduria. Chronic occupational exposure to lead, or consumption of illicit alcohol adulterated with lead, has also been linked to a high incidence of renal dysfunction, which is characterized by glomerular and tubulointerstitial changes resulting in chronic renal failure, hypertension, hyperuricemia, and gout. A high incidence of nephropathy was reported during the early part of this century from Queensland, Australia, in persons with a history of childhood lead poisoning. No such sequela has been found in studies of three cohorts of lead-poisoned children from the United States. Studies in individuals with low-level lead exposure have shown a correlation between blood lead levels and serum creatinine or creatinine clearance. Chronic low-level exposure to lead is also associated with increased urinary excretion of low molecular weight proteins and lysosomal enzymes. The relationship between renal dysfunction detected by these sensitive tests and the future development of chronic renal disease remains uncertain. Epidemiologic studies have shown an association between blood lead levels and blood pressure, and hypertension is a cardinal feature of lead nephropathy. Evidence for increased body lead burden is a prerequisite for the diagnosis of lead nephropathy. Blood lead levels are a poor indicator of body lead burden and reflect recent exposure. The EDTA lead mobilization test has been used extensively in the past to assess body lead burden. It is now replaced by the less invasive in vivo X-ray fluorescence for determination of bone lead content.     

Hyperuricemia

Uric acid is formed by catabolism of purine nucleotides. Approximately 25% is excreted through the intestines and the rest through the kidneys. A little less than 5% of the population in western industrialised countries have hyperuricaemia, primarily men and postmenopausal women. Hyperuricaemia is in most cases caused by reduced renal excretion, which may be idiopathic with otherwise normal renal function. But the condition is often associated with hypertension, nephropathy and treatment with diuretics and certain other drugs. Hyperuricaemia due to increased purine metabolism is seen in malignant haematological diseases, other conditions with increased cellular turnover and during initiation of chemotherapy in malignant diseases. Moreover hyperuricaemia is associated with some metabolic disturbances and risk factors of atherosclerotic cardiovascular disease including hypertension, overweight, insulin resistance and hyperlipidaemia. Hyperuricaemia is rarely caused by constitutional enzymatic abnormalities influencing purine metabolism. In most cases hyperuricaemia is asymptomatic. It may though be complicated by gout, urolithiasis and possibly gouty nephropathy. The risk of complications is correlated to the degree and duration of hyperuricemia. Consequently, measures to affect predisposing and associated conditions should be taken including weight reduction, physical exercise and diet guidance, treatment of hypertension and possibly changes in medication. Urate lowering drug treatment is normally not indicated in asymptomatic hyperuricaemic individuals.     

Renal hypertension in children

Preliminary results of this retrospective-prospective analysis of renal hypertension in 110 children indicate that hypertension may be secondary to a wide variety of acute progresive, and chronic renal diseases which may be either congenital or acquired. Affected children may be detected at any time from infancy through adolescence. Symptoms usually associated with acute glomerulonephritis (i.e., headache, swelling, nausea, vomiting, anorexia, fatigue, dizziness, and fever) occur in both acute and chronic renal diseases associated with hypertension. Headache and swelling are the most common symptoms in this series. Peripheral edema, rales, and increased heart size were found in between 10 and 25% of these children. Differential diagnosis may be approached by a consideration of causes of acute and chronic hypertension. The child with chronic renal disease usually presents with a long history of fatigability, poor growth, and pallor, and laboratory tests reveal elevation of the creatinine and BUN along with anemia, hypocalcemia, and hyperphosphatemia. In contrast, the child with acute renal disease and hypertension presents with a history of prior good health followed by the abrupt onset of signs and symptoms of renal disease; laboratory tests usually reveal modest elevations of creatinine and BUN, anemia is unusual, an abnormal urinalysis is common, and serum calcium and phosphorous levels are usually normal. Renovascular and asymmetric renal parenchymal disease represent uncommon but important conditions because surgery may be curative. Treatment may be surgical, medical, or combined. Surgical conditions include renal trauma, hydronephrosis, asymmetric renal disease, and renal arterial disease. Adequate blood pressure control without medication can be expected following surgery in instances of unilateral involvement with a normal contralateral kidney. Meticulous assessment of the contralateral kidney is needed to determine that it is normal. If surgery is unsuccessful or is not indicated, pharmacologic therapy is initiated with a stepwise regimen starting with the mildest agent (e.g., thiazides) and then adding additional antihypertensive drugs when adequate blood pressure control has not yet been achieved. The goal of therapy is the lowest, safest, tolerated blood pressure levels. Long-term, carefully designed studies of antihypertensive agents for children with renal hypertension are not available. The need for collection and critical analysis of data concerning the clinical course of children with renal hypertension is evident from a review of the literature and from the preliminary data presented in this series. The presentation of such information and a critique of outcome variables will provide a basis for program planning for affected children and improvement in patient care where indicated.     

Experimental and human nephrotoxicity induced by ochratoxins

Ochratoxin A is a mycotoxin: a dihydroisocoumarin derivative linked to L. beta phenylalanine. Ochratoxin A is produced by a number of Aspergillus and Penicillium species. This mycotoxin is a carcinogenic, teratogenic, mutagenic and immunosuppressive substance. Ochratoxin A is a common contaminant found in a variety of foods for human nutrition as well as animal feeds. The aim of this study is to discuss nephrotoxic properties of this mycotoxin in humans. Nephrotoxicity has been reported in many animals after exposure to ochratoxin A. Porcine nephropathy due to this mycotoxin is a well known disease characterized by impairment of proximal renal function. Renal damage is also confined to the proximal tubule in other animal species. A good correlation is found between renal function abnormalities and the location of the lesions along the nephron. Of particular interest is the presence of nuclear abnormalities of the epithelial cells with pyknosis, karyorrhexis and karyomegaly. The question is to know if ochratoxin is nephrotoxic in humans. Acute nephrotoxicity seems to be very rare and we found only one case report suggesting such a possibility. We observed the occurrence of chronic renal failure in two patients with a possible responsibility of a chronic ochratoxin A intoxication. Clinical and histologic findings in these two patients were quite similar to those described in several cases of karyomegalic interstitial nephritis. Striking similarities between the changes in renal structure and function seen in ochratoxin A-induced experimental nephropathies and in Balkan endemic nephropathy suggest a common etiologic agent. This mycotoxin could be also responsible for interstitial nephropathies in North Africa.     

Diagnostic and therapeutic management of ethylene glycol poisoning. Importance of crystalluria. Apropos of a case

During the course of a case of ethylene glycol poisoning with ensuing oliguric renal failure despite early dialysis, we show the importance of early diagnosis of this intoxication in underlined. Characteristics of ethylene glycol poisoning are: metabolic acidosis with anion gap (without lactic acidosis or keto-acidosis) and high plasma osmolarity. Awaiting the result of blood and urinary toxic values, crystalluria, by typical needle monohydrate calcium oxalate crystals finding, evokes the diagnosis and permits to start a specific treatment. This treatment is based on: principles of intensive care, ethanol administration (or 4-methyl-pyrazole now available), also thiamine and pyridoxine administration and finally, dialysis therapy. We can hope, with early and intensive management of this poisoning, to prevent the renal failure, principal complication of ethylene glycol ingestion, which can lead to chronic renal failure. Therefore, crystalluria, an easy and specific diagnosis technic, is of great interest.     

Acute arterial hypertension caused by dissecting aneurysm of the renal artery

BACKGROUND: Aneurysm of the renal artery is an uncommon discovery at arteriography performed as part of a hypertension work-up. CASE REPORTS: We observed acute hypertension following dissection of a renal artery aneurysm which led to circulating channel stenosis. After surgical correction of the lesion, arterial pressures returned to normal. DISCUSSION: Most cases of renal artery aneurysm do not cause hypertension. In such cases, the high blood pressure is idiopathic or related to fibrodysplastic stenosis of the renal artery often associated with aneurysm formation. In rare cases with obstructive complications alone an aneurysm may lead to acute hypertension either after dissection as in our case or after thrombus formation. Surgery is generally required.     

ber die laquo;Omnipotenz> der Chelattherapie

About the 'Omnipotence' of the Chelation Therapy In the eighties the 'method of treatment proven in many thousands of cases over 20 years' was transferred from the USA to Germany (enjoys a priori considerable faith) using very dubious promises. It was Clarke et al. who introduced this 'therapy' in 1955. The dubious promise was to maintain that the chelation therapy eliminates or alleviates symptoms in the case of the following illnesses: Alzheimer's disease, senility, schizophrenia, rheumatoid arthritis, osteoarthritis, gout, renal calculus, apoplectic coma, gallstones, multiple sclerosis, osteoporosis, chronic fatigue syndrome, varicose veins, hypertension, failure of memory, scleroderma, Raynaud's disease, digitalis intoxication, intermittent claudication, diabetic ulcer, disturbance of the blood supply, ulcer on the legs, snake poison, impotence, emotional difficulties, defective hearing, vision disorder. There is not the slightest proof of effectiveness for any of the listed indications. The burden of proof lies with the supplier. Even in the case of the relatively often examined peripheral atherosclerotic changes (claudicatio intermittens) there is no proof that EDTA has a greater effect than placebo. For coronary heart disease too there is no evidence for any usefulness of the chelation therapy beyond that of a placebo effect. Only controlled studies can help to improve the therapy in the sense of 'Evidence-based medicine'. Retrospective investigations on thousands of patients cannot 'prove' anything, although this is maintained again andagain.     

Clinical and histopathologic examination of renal allografts treated with tacrolimus (FK506) for at least one year

BACKGROUND: We clinically and pathologically analyzed renal allografts from 1 9 renal transplant patients treated with tacrolimus (FK506) for more than 1 year. METHODS: Twenty-six renal allograft biopsy specimens from 1 9 renal transplant patients who underwent transplantations between 1991 and 1993 were evaluated. Thirteen biopsies were performed from stable functioning renal allografts with informed consent (nonepisode biopsy) and the other 13 were from dysfunctional renal allografts with a clinical indication for biopsy (episode biopsy). RESULTS: The main pathologic diagnoses (some overlap) were acute rejection (AR; n = 4), chronic rejection (CR; n=5), AR+CR (n =4), recurrent IgA nephropathy (n =5), normal findings (n =2), minimal-type chronic FK506 nephropathy (n = 9), and mild-type FK506 nephropathy (n = 11). Of the nonepisode biopsies, 7 and 4 biopsies showed minimal-type and mild-type chronic FK506 nephropathy, respectively. Chronic FK506 nephropathy consisted of rough and foamy tubular vacuolization (5 biopsies), arteriolopathy (angiodegeneration of the arteriolar wall; 20 biopsies), focal segmental glomerulosclerosis (4 biopsies) and the striped form of interstitial fibrosis (11 biopsies). The serum creatinine levels of patients in the mild-type chronic FK506 nephropathy group, which included 7 episode biopsies, were statistically higher than those in the minimum-type chronic FK506-nephropathy group (P< 0.001). CONCLUSIONS: This study demonstrates that chronic FK506 nephropathy consists primarily of arteriolopathy manifesting as insudative hyalinosis of the arteriolar wall, and suggests that mild-type chronic FK506 nephropathy is a condition which may lead to deterioration of renal allograft function.     

Thin GBM nephropathy: premature glomerular obsolescence is associated with hypertension and late onset renal failure

Thin glomerular basement membrane (GBM) nephropathy, also called familial benign hematuria, is characterized by chronic hematuria and uniform thinning of the lamina densa of the glomerular basement membrane. It generally holds an excellent renal prognosis. Alport syndrome in early stages can also show attenuation of the GBM; conversely, renal insufficiency has been reported in familial benign hematuria. To discern early Alport syndrome from thin GBM nephropathy, we carried out a prospective epidemiological study in which 19 normotensive and non-azotemic adult patients with chronic microscopic (18 of 19) and macroscopic (1 of 19) hematuria and biopsy-proven thin GBM nephropathy were followed for a median of 12 years (range 9 to 15 years). Renal biopsies of thin GBM patients at entry showed an increased incidence of focal global glomerulosclerosis when compared to disease controls as IgA nephropathy (P = 0.047) and normal renal tissue (P = 0.0075). All renal biopsies showed the presence of the Goodpasture antigen when tested immunohistochemically. Presence of Alport syndrome was excluded clinically as none of the patients had complaints of hearing loss or abnormalities by audiography and ophthalmology. At the end of follow-up, the incidence of hypertension in thin GBM nephropathy (35%) exceeded that of healthy clinical controls (P = 0.048), and one hypertensive patient developed mild renal failure. In the normotensive patients, the glomerular filtration rate at follow-up as measured by inulin clearance was reduced in three out of seven; these were over 50 years of age. Although no family members were known to have renal disease at inclusion, within four families six elderly first degree relatives had developed unexplained renal insufficiency at the end of follow-up. Thus, thin GBM nephropathy predisposes to premature glomerular obsolescence, leading in time to increased incidences of hypertension and late onset renal insufficiency.     

Severe lead poisoning caused by an ingested fishing weight

Authors describe the case-history of a 17 year old male who accidentally ingested a fishing weight that was retained in the stomach and caused a serious lead poisoning. It is worth mentioning that beside the wellknown symptoms and signs of lead intoxication also the liver was seriously affected. The histologically verified toxic lesion of the liver presumably can be attributed to the large quantities of lead absorbed within a short period. This also explains the appearance of symptoms and signs indicating to encephalopathy beside the young age of the patient. The foreign body could not be removed by means of gastroscopy, therefore a gastrotomy was carried out followed by chelating treatment with i.v. CaNa2EDTA that resulted in complete clinical and laboratory recovery. The case history draws the attention to the importance of the quick removal of the retained lead containing objects out of the gastrointestinal tract.     

Dietary magnesium supplementation attenuates ethanol-induced myocardial dysfunction

Hypomagnesemia is positively correlated with a number of cardiovascular abnormalities and recent evidence suggests that magnesium supplementation prevents ethanol-induced development of hypertension. The purpose of our study was to assess whether dietary magnesium supplementation effectively reverses or attenuates chronic ethanol-induced cardiac dysfunction, both at the tissue and the cellular level. Therefore, the influence of dietary magnesium supplementation during chronic ethanol ingestion on the mechanical properties of cardiac muscle was studied using isolated papillary muscles and ventricular myocytes from rat heart. In addition, the acute effects of ethanol on cardiac muscle from animals chronically exposed to ethanol in the absence and presence of dietary magnesium supplementation were also examined. Chronic ethanol exposure caused significant cardiac, hepatic, and renal enlargement, increased systolic blood pressure, and produced hypomagnesemia. After chronic ethanol exposure, the baseline force generating capacity of papillary muscles was markedly depressed and was associated with a significant slowing in the maximum velocities of contraction and relaxation. By contrast, in isolated myocytes, long-term ethanol exposure increased the extent of cell shortening associated with a significant reduction in the duration of relengthening and an increase in both the maximum velocities of shortening and relengthening. Dietary magnesium supplementation among animals chronically ingesting ethanol effectively normalized heart size, systolic blood pressure, and reduced plasma ethanol concentration. Magnesium supplementation also attenuated chronic ethanol-induced depression of contractile force and increased the extent of cell shortening. As expected, acute ethanol exposure caused a dose-dependent inhibition of both isometric force and isotonic shortening associated with a decrease in the intracellular calcium transient. However, the extent of the acute ethanol-induced reduction in isometric force and isotonic shortening was always slightly greater among preparations from animals chronically exposed to ethanol. Dietary magnesium supplementation normalized the acute inhibitory action of ethanol on isometric force, isotonic shortening, and the intracellular calcium transient. Our results suggest that dietary magnesium supplementation may attenuate chronic ethanol-induced alterations in baseline myocardial mechanical function and normalize the cardiac response to acute ethanol exposure.     

Hemoperfusion with coated activated charcoal for treating acute poisoning by remedies, plant protectants, and fungi. I. Remedies (author's transl)

Hemoperfusion with coated activated charcoal is a novel procedure for treating acute poisoning. It enables the elimination of both, water-soluble and liposoluble toxins. Hemoperfusion with coated activated charcoal has proved to be superior to hemodialysis in the treatment of barbiturate or bromocarbamide poisoning both under experimental conditions as well as in the ward. Analogous statements may be made for the therapy of glutethimide poisoning. Methaqualone, on the other hand, could not be eliminated sufficiently well in animal trials. Intoxications by "mild" analgetics, such as paracetamol and acetylsalicylic acid, may be treated successfully with hemoperfusion. Treatment of acetylsalicylic acid poisoning is equally effective with hemoperfusion as with hemodialysis. Prospects for the success of hemoperfusion in treating intoxication from tricyclic antidepressants and neuroliptics are slight. It is simply the danger of antidepressant poisoning that justifies using this method of treatment in the first few hours after ingestion in order to reduced the flow of the psychopharmaceutical substance into the tissue.     

Current problems of lead poisoning]

In collaboration with private associations and public services, we screened a targeted population for serum lead levels and observed lead poisoning (serum Pb > 100 micrograms/l) in 6 out 44 children living in precarious conditions in Poitiers, France. This observation underscores some of the major problems encountered in the battle against lead poisoning in western countries. First, the social, economical or legal situation of the population at risk often results in exclusion from the normal health care network. If after a coordinated effort based on mutual trust, children exposed to lead poisoning can be identified, the second problem is to identify the source of intoxication. Scaling paint in the current housing may be incriminated, but how can the true source be identified when the populations concerned change residence often and may be unwilling to disclose their previous residence due to fear of reprisals for themselves or the new occupants? And if the source is identified, the cost of rehabilitation or the illegal situation of the family may raise further problems requiring adapted solutions. The prevention of lead poisoning calls for a targeted screening program, combined efforts of public authorities and health care workers, and close cooperation with private associations. All intoxicated children should be removed from the source of exposure and their families protected from the risk of sanctions. Only an active and practical public health policy can provide the solution to this continuing public health problem.     

Gouty arthritis in nodal osteoarthritis

OBJECTIVE: To analyze the clinical features and identify factors associated with the development of gouty arthritis in nodal osteoarthritis (OA). METHODS: Thirty-two consecutive patients (21 women and 11 men, mean age 75.8 years) with both nodal OA and crystal proven acute gout and/or tophi of distal/proximal interphalangeal (DIP/PIP) joints were studied between 1986 and 1994. RESULTS: Tophi of DIP and/or PIP joints were present in 29 (90%) patients; alone in 9 and together with acute DIP or PIP gouty arthritis in 20. Three patients had acute DIP or PIP gouty episodes but no digital tophi. Mean pretreatment serum urate was 614.9 +/- 163.2 (range 422-1088 mumol/l). Risk factors for gout included diuretic use (81%), renal failure (59%), hypertension (66%), alcoholism (22%), prophylactic low dose ASA (20%), and a positive family history (16%) of patients. CONCLUSION: The coexistence of gouty arthritis in nodal OA is important to recognize and treat, particularly in elderly women with renal failure, hypertension, or cardiac failure who are receiving longterm diuretic therapy.     

Hypertension in insulin-dependent diabetes

Hypertension is seen in approximately 85% of IDDM patients with diabetic nephropathy and blood pressure elevation is an early event in the development of this complication. In IDDM patients with clinical nephropathy, a positive correlation has been demonstrated between the blood pressure and the urinary albumin excretion and reduction of blood pressure reduces albuminuria as well as the rate of decline in glomerular filtration rate. Also extrarenal abnormalities such as retinopathy, cardiovascular diseases and signs of endothelial dysfunction, sometimes seen in non-diabetics with severe and/or prolonged hypertension, are frequently demonstrated in IDDM patients with clinical nephropathy. The aim of the present study was to provide circumstantial evidence for the thesis that hypertension in IDDM patients with nephropathy is secondary to the kidney involvement and not the cause of the kidney disease. Furthermore, by familial and physiological studies the review also aimed to contribute to the understanding of the pathogenesis of hypertension in patients with clinical nephropathy. Finally the question of optimal pharmacological antihypertensive treatment was discussed. It was demonstrated that in IDDM patients with elevated urinary albumin excretion above normal level the prevalence of hypertension is 60%, whereas in patients without signs of renal impairment hypertension is not more prevalent as in the age and sex-matched background population (about 4% in both groups). Based upon the observation, that some of these IDDM patients with hypertension but normal UAE were hypertensive for many years, we designated this group as IDDM patients with essential hypertension for further studies. In this group, we had the opportunity to study the association between blood pressure and the development of extrarenal complications in patients with IDDM. The group with essential hypertension and IDDM showed to have less retinopathy compared with diabetics with similar blood pressure but elevated UAE. In contrast to the hypertensive patients with nephropathy, a normal transcapillary escape rate of albumin and normal plasma levels of von Willebrand factor, of angiotensin-converting-enzyme and of inactive renin were demonstrated in the former group of patients. Thus, the extrarenal abnormalities found in IDDM patients with hypertension are more closely associated to the presence of albuminuria than to the elevation of blood pressure, indirectly supporting the hypothesis that hypertension per se is not the cause of these abnormalities in the IDDM patients with nephropathy. Furthermore, the present study does not disclose a genetic disposition to hypertension in IDDM patients with elevated UAE.     

Ethnicity, hypertension, coronary heart disease and renal diseases in South Africa

This paper reviews the impact of race and environment upon hypertension, coronary heart disease and renal diseases in South Africa. Inequalities of socioeconomic status, lifestyle, and access to South African health care have produced striking differences in the prevalence and complications of hypertension. Coronary heart disease is 'epidemic' in the white and Indian population and is still relatively uncommon in blacks. There are different histological patterns of glomerulonephritis among the racial groups, which may lead to end-stage renal disease. Hypertension is an important cause of end-stage renal disease in the black population whilst analgesic nephropathy is important in the white population. Efforts are now being made to comprehend these daunting realities and to minimize the inequalities.     

Effect of manual segmental vibration on neuromuscular excitability

The prevalence of amphetamine abuse and the frequency of emergency department visits for amphetamine intoxication have increased dramatically worldwide. In this study, we retrospectively investigated the relationship between the prognostic features and clinical manifestations among patients admitted to the emergency department of a university hospital for acute methamphetamine intoxication during a 6-year period. Data collected included gender, age, route of abuse, time between drug exposure and arrival at the emergency department, estimated dose, signs and symptoms, laboratory values, and complications. Emergency therapy and cooling procedures were also recorded. After excluding 26 patients with multiple-drug intoxication, 18 patients (male-to-female ratio, 11:7) were include in the analysis. The mean age was 25.6 years. Thirteen patients survived and five died. Patients who died often presented with coma (80% vs 0%, p = 0.002), shock (60% vs 8%, p = 0.044), convulsions (100% vs 23%, p = 0.007), oliguria (80% vs 0%, p = 0.002), and high body temperature (41.4 +/- 0.5 degrees C vs 39.4 +/- 2.1 degrees C, p = 0.005). Furthermore, patients who died had significantly higher concentrations of blood urea nitrogen (8.7 +/- 2.1 vs 5.6 +/- 2.0 mmol/L, p = 0.01) and serum creatinine (212 +/- 71 vs 115 +/- 27 mumol/L, p = 0.033), and lower values of arterial pH (7.12 +/- 0.12 vs 7.34 +/- 0.10, p = 0.03), than those who survived. In the fatality group, the most common complication was rhabdomyolysis with acute renal failure (5 of 5); multiple organ failure resembling that from heatstroke was the leading cause of death from acute methamphetamine intoxication. In conclusion, the adverse prognostic features in patients with acute methamphetamine intoxication include coma, shock, convulsion, oliguria, and high core temperature. Acidosis, volume depletion, and ischemic renal damage were potential risk factors for development of acute renal failure in these patients.     

Mobilization of lead by calcium versenate and dimercaptosuccinate in the rat

1. Calcium disodium ethylenediaminetetraacetate (CaNa2 EDTA) and meso-2,3-dimercaptosuccinic acid (DMSA) individually and in permutation-combination in various doses (0.1, 0.2 and 0.4 mmol/kg bodyweight) were investigated for their efficacy to mobilize lead from vital tissues into urine and faeces and to restore the lead-sensitive biochemical parameters in lead pre-exposed rats with a view to develop the most acceptable treatment regimen for lead poisoning with a minimal loss of endogenous essential elements. 2. The combined therapy was more effective than a single chelator treatment. 3. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA caused a lower depletion of zinc, calcium and iron but possessed almost equal capability to that of 0.4 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA to produce urinary as well as faecal excretion of lead, to reduce the tissue burden of lead, including that of the brain, and to reverse lead-induced biochemical alterations. 4. The combination of 0.2 mmol/kg CaNa2EDTA + 0.4 mmol/kg DMSA has shown a definite improvement over previously reported combinations in terms of removal of lead from tissues, particularly the brain, restoration of urinary delta-aminolevulinic acid levels and a decrease in the loss of body zinc and is, therefore, recommended for the treatment of lead intoxication.     

Reversed midgut rotation in a neonate: case report with a brief review of the literature

The epidemiological evidence that only a subset of diabetic patients are susceptible to renal damage and the demonstration of clear familiar clustering of diabetic nephropathy are consistent with the possibility that genetic factors may explain the liability to or protection from renal disease of diabetic patients. A predisposition to hypertension and cardiovascular disease may be an important determinant of susceptibility to renal disease and its cardiovascular complications in diabetes since raised blood pressure [1] and an increased frequency of cardiovascular disease [2] are more prevalent in parents of diabetic patients with nephropathy. These results have raised growing interest in the search for intermediate phenotypes significantly associated with diabetic nephropathy, poorly influenced by environment, stable with age, easy to quantify and possibly dependent upon a single major gene effect. Such intermediate phenotypes can be useful for early diagnosis and would help clarify the molecular mechanisms leading to diabetic nephropathy. An elevation of Na+/H+ antiporter activity has consistently been associated with diabetic renal disease both in insulin-dependent diabetes mellitus (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM) patients, making this cell membrane exchanger system an ideal intermediate phenotype for the study of diabetic nephropathy.     

A study of mortality and urinary excretion of oxalate in male rats following acute experimental intoxication with diethylene-glycol. Preliminary report

Acute intoxication by diethylene glycol (LD 50) in male rats is associated with a considerable urinary excretion of oxalate, which is significantly decreased by alkalinisatin and/or intraperitoneal injection of ethanol with hydration. Mortality during the five days following intoxication is significantly decreased by major hydration only or together with pyridoxine administration, but is cancelled by major hydration together with alkalinisation or intraperitoneal administration of ethanol, plus hydration, with or without alkalinisation. -- It might be inferred that diethylene glycol has the same metabolic pathway as ethylene glycol and treatment of acute intoxication by diethylene-glycol should be the same as that of acute poisoning with ethylene glycol.