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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.
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PMID:Renal hypertension in children. 99 44

Thirty-eight workers from a factory producing nickel-cadmium and other types of batteries came to us for medical evaluation. They included 21 women and 17 men (seniority 2-20 years, age range 31-63 years), and represented a self-selected subset of 700-900 ever-employed and 200+ recently or currently employed workers in the factory. Thirty-four worked on the nickel-cadmium assembly line. Symptoms and signs included: headache in 34; weakness, fatigue and lassitude in 26; dizziness in 16; pruritus and skin eruptions in 37; gingivitis, teeth loss and caries in 34; nasal congestion, nosebleeds and anosmia in 30; cough, phlegm production, wheezing and shortness of breath in 26; "asthma" in 14; bone pain in 18; urinary frequency, beta 2 microglobulinuria and kidney stones in 17; and sterility or multiple abortions (33) in 8 of 21 women. One additional patient had died from an "amyotrophic lateral sclerosis-like syndrome", while CT scans in six workers revealed brain atrophy. One other worker had leukemia, and two had died from cancer (lung and pancreas). Those who had worked for more than 10 years had more symptoms and signs than shorter-term employees, especially neurological illness, bone pain and urinary tract problems, including beta 2 microglobulinuria. Past blood and urinary cadmium levels were in the range of 1.6-8.7 micrograms/dl and 8-306 micrograms/l, respectively. Our findings indicated that: a) health risks for workers were not confined to the nickel-cadmium assembly line or to older workers, b) hazardous exposures still existed and illness appeared in new workers after a clean-up and intervention program, and c) exposures involved increased risks for renal disease and cancers. Finally, there is a need to control exposures and determine health risks in the full cohort of those ever employed, in the workers' children, and in the surrounding environment (air, ground, water) due to the dumping of waste from the plant.
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PMID:Medical findings in nickel-cadmium battery workers. 142 13

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

Computed tomographic (CT) findings of cerebral and cerebellar calcification are described in three American adults with raised serum lead levels and known exposure to lead for 30 or more years. Calcification patterns were punctiform, curvilinear, speck-like, and diffuse and were found in the subcortical area, basal ganglia, vermis, and cerebellum. Admission serum lead levels ranged from 54 to 72 micrograms/dl (normal, 0-30 micrograms/dl). Nonspecific neurologic manifestations consisted of dementia, diminished visual acuity, peripheral neuropathy, syncope, dizziness, nystagmus, easy fatigue, and back pain. Two patients developed chronic renal disease and hypertension; in both cases, serum parathormone was elevated. Blood, calcium, and phosphorus were normal in all three. No other structural abnormalities were observed with CT. Although the pathophysiologic mechanism of these findings remains poorly understood, it is suggested that chronic lead exposure should be included in the differential diagnosis of unexplained intracranial calcifications in adults.
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PMID:Intracranial calcification in adults with chronic lead exposure. 348 74

A 19-year-old woman with insulin-dependent diabetes mellitus (IDDM) of 3.5 years duration had been suffering from recurrent episodes of diabetic ketoacidosis (DKA), dizziness, and weight loss (16 kg, 29%) for 6 months. History and physical examination gave evidence of severe peripheral and autonomic neuropathy. Radionuclide retention on gastric emptying test at 60 min was greater than 90% (normal < 60%). On autonomic cardiovascular testing there was evidence of both parasympathetic and sympathetic damage. There was no evidence of nephropathy or retinopathy. Optimal diabetic control using 4 insulin injections (2 u/kg/day) and high-dose cisapride terminated the vomiting, and she regained the weight lost within 5 months. This case is unique in that severe diabetic neuropathy followed relatively soon after onset of disease, without other microvascular complications. The correct diagnosis of gastroparesis as the cause of the recurrent DKA and weight loss, and the specific prokinetic therapy and nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Specific prokinetic therapy and the nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Gastroparesis can cause recurrent DKA even in young patients with IDDM of short duration.
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PMID:[Severe neuropathy in a young diabetic]. 784 56

Seventy-five non-dialized patients with chronic renal failure (CRF) and severe renal anemia were enrolled in a study, receiving r-HuEPO subcutaneously thrice weekly for 6 months. In 64 patients (85%) 7 weeks of treatment with a weekly dose of 158 U/kg were required to achieve Hb concentrations within the target range of 10 to 12 g/dl. Of the 11 patients (15%) who failed to achieve the target Hb range, none were considered to be non-responders as they were excluded for unrelated reasons prior to week 16 (8 cases), or were iron deficient (2 cases), or had bleeding complications (1 patient). Maintaining the Hb concentration at a level of 10.5 g/dl required a mean r-HuEPO dose of 92 U/kg per week. Adverse events were generally mild or moderate. The most commonly reported were hypertension (8%), viral infection/including flu-like syndrome (7%), nausea (7%), and dizziness (5%). Statistically significant increases in mean creatinine concentrations observed after 12 and 24 weeks were most likely due to the progression of renal disease. These results confirm that 50 U/kg of r-HuEPO given 3 times per week subcutaneous provide a safe and effective therapy for anemic predialysis patients.
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PMID:Effectiveness and safety of recombinant human erythropoietin (r-HuEPO) in the treatment of anemia of chronic renal failure in non dialysis patients. European Multicentre Study Group. 807 Sep 41

Epalrestat is a carboxylic acid derivative which inhibits aldose reductase, an enzyme of the sorbitol (polyol) pathway. Under hyperglycaemic conditions epalrestat reduces intracellular sorbitol accumulation, which has been implicated in the pathogenesis of late-onset complications of diabetes mellitus. Epalrestat 150 mg/day for 12 weeks improved motor and sensory nerve conduction velocity, and vibration threshold compared with baseline and placebo in patients with diabetic neuropathy. Subjective symptoms including pain, numbness, hyperaesthesia, coldness in the extremities, muscular weakness, dizziness, and orthostatic fainting were also improved. Similar benefits were seen in a comparison with historical controls. Epalrestat 300 mg/day for 1 or 3 years was also significantly superior to placebo or no treatment in improving electroretinogram parameters and photo stress recovery time in patients with diabetic retinopathy. Improvements were also documented by funduscopy and fluorescein angiography. Epalrestat appeared most effective in patients with less severe diabetes mellitus and more recent development of late-onset complications. Epalrestat is apparently well tolerated with predominantly minor adverse events reported in clinical trials. Liver enzyme elevations were most commonly reported but generally resolved spontaneously on dose reduction or discontinuation. The effects of age and renal impairment on the efficacy and tolerability of epalrestat require clarification, and data on its use in other late-onset complications of diabetes such as nephropathy are also lacking. Comparisons with other aldose reductase inhibitors are also required to fully determine the role of epalrestat. The suggested ability of epalrestat to prevent the onset of diabetic complications should also be investigated. Thus, available data suggest epalrestat produces some improvement in the late-onset neuropathy and retinopathy associated with diabetes mellitus, although additional trials are required to determine whether ongoing therapy is necessary to maintain the improvements achieved and to confirm tolerability in the long term. Nevertheless, preliminary results suggest that epalrestat may be a useful drug in an area where there is a need for effective therapy.
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PMID:Epalrestat. A review of its pharmacology, and therapeutic potential in late-onset complications of diabetes mellitus. 831 78

A cross-sectional study was designed to identify a relationship between the presence of symptoms usually related to nervous system involvement as well as other chronic complications of diabetes with three objectively defined degrees of autonomic neuropathy (AN). Symptoms usually related to peripheral sensitive neuropathy and AN were assessed using a questionnaire applied to 132 diabetics (38 IDDM and 94 NIDDM), 65 without and 67 with AN. AN was classified as follows according to 5 cardiovascular autonomic tests described by Ewing: 1) early involvement-1 abnormal test (N = 27); 2) definite involvement-2 or 3 abnormal tests (N = 26); 3) severe involvement-4 or 5 abnormal tests (N = 14). A statistically significant association was observed between degree of autonomic involvement and the presence of the following symptoms: dizziness on standing, dysphagia, vomiting, diarrhea, fecal incontinence, gustatory sweating, urinary retention, numbness and hyperesthesia of the feet or legs. Constipation and cystitis were not significantly related to cardiovascular AN. Only 3% of the patients without neuropathy and with early involvement had four or more than four of the symptoms. The prevalence of proliferative retinopathy and nephropathy was increased among patients with more severe degrees of AN. For IDDM patients there was a positive correlation between the degree of cardiovascular AN and the duration of diabetes. We conclude that: 1) severe cardiovascular AN is usually related to 4 or more of the evaluated symptoms and those patients usually have the other complications of diabetes; 2) severe AN could be a risk factor or an indicator of the same underlying process that determines the beginning of proliferative retinopathy and/or nephropathy.
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PMID:Relationship between the degree of cardiovascular autonomic dysfunction and symptoms of neuropathy and other complications of diabetes mellitus. 858 Aug 65

Losartan potassium is the first of a new class of orally active antihypertensive drugs which antagonise the action of angiotensin (AT) II at the AT1 receptor subtype. Losartan potassium is converted by the liver to the active metabolite E-3174, which is a more potent antagonist at the AT1 receptor. E-3174 is responsible for most of the pharmacological effects of losartan potassium, and its long half-life contributes to the extended duration of action of the drug. Losartan potassium is effective as a once-daily antihypertensive agent. In mild to moderate hypertension, losartan potassium has similar efficacy to enalapril, atenolol and felodipine extended release. When losartan potassium is combined with hydrochlorothiazide there is a further reduction in blood pressure. Losartan potassium is well tolerated in mild, moderate and severe essential hypertension, with dizziness being reported as the only drug-related adverse effect. The overall rate of patient withdrawal from therapy due to adverse experiences with losartan potassium is lower (2.3%) than that of placebo (3.7%). First-dose hypotension is uncommon, perhaps due to the slower onset of action of the drug, and cough does not appear to be a significant problem. A number of areas concerning the safety and efficacy of losartan potassium remain to be clarified. In particular, long term tolerability studies are needed; cough only became apparent as an adverse effect of ACE inhibitors after 3 to 4 years of use. Postmarketing surveillance has shown that angioedema, a rare but life-threatening adverse effect of ACE inhibitors, also occurs with losartan potassium. Further data are needed on the use of losartan potassium in patients with renal impairment before accepting the recommendation that dosage adjustment is not necessary. The pharmacokinetics and pharmacodynamics of losartan potassium in patients with hepatic disease also require further investigation. Losartan potassium increases uric acid secretion and lowers plasma uric acid levels, which may be of benefit when losartan potassium is combined with a thiazide diuretic, but which may otherwise lead to uric acid stone formation and possibly to nephropathy. Simple control of blood pressure is no longer an adequate goal in the management of hypertension. Any new antihypertensive agent should also reduce cardiovascular events, prevent or cause regression of end-organ damage such as left ventricular hypertrophy, atherosclerosis and renal failure, and should not impair quality of life. Such data on losartan potassium are not currently available. Losartan potassium is likely to be used in patients who are intolerant of ACE inhibitors, but its future in the management of hypertension will depend on long term tolerability studies and data on its effects beyond simple blood pressure control.
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PMID:A risk-benefit assessment of losartan potassium in the treatment of hypertension. 901 Jun 43

Symptomatic hypotension during hemodialysis is a disabling complication in end-stage renal disease (ESRD) patients, especially in certain groups of patients who are at higher risk for this problem. Autonomic dysfunction is thought to play a significant role. We evaluated the efficacy of midodrine, an oral agent with selective alpha-adrenergic agonist activity used in the treatment of neurogenic orthostatic hypotension, on 10 hemodialysis patients with persistent intradialytic hypotension. The patients were given a dose of midodrine (mean dose, 5.5 mg; range, 5 to 10 mg) 30 minutes before each hemodialysis session. We compared blood pressure, pulse, body weight, and laboratory values for 10 consecutive dialysis sessions off and on midodrine therapy. There was a statistically significant improvement in lowest intradialytic systolic blood pressure (from 96.6 to 114.7 mm Hg; P < 0.001), lowest intradialytic diastolic blood pressure (from 53.2 to 59.0 mm Hg; P = 0.002), lowest intradialytic mean arterial pressure (from 67.7 to 77.6 mm Hg; P < 0.001), posthemodialysis systolic blood pressure (from 116.5 to 127.1 mm Hg; P < 0.001), posthemodialysis diastolic blood pressure (from 66.6 to 69.7 mm Hg; P = 0.040), and posthemodialysis mean arterial pressure (from 83.2 to 88.8 mm Hg; P = 0.001) after patients were placed on midodrine. There also was a small but statistically significant decrease in intradialytic pulse rate (from 86.3 to 81 beats/min; P = 0.021) and posthemodialysis pulse rate (from 87.4 to 81.7 beats/min; P = 0.024) after initiation of midodrine therapy. There was no significant difference in any of the prehemodialysis blood pressure measurements or pulse rate off or on midodrine therapy. The improvements in intradialytic and posthemodialysis blood pressure were associated with a uniform subjective improvement in symptoms associated with dialysis hypotension, such as cramps, fatigue, dizziness, and weakness. Other than scalp paresthesia in one patient, no adverse effects were noted. Our results suggest that the administration of a single dose of midodrine before hemodialysis is an effective therapy for intradialytic hypotension. A prospective trial with adequate patient numbers and long-term follow-up would be useful to evaluate this drug's efficacy and safety profile in patients with ESRD.
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PMID:Intradialytic hypotension: is midodrine beneficial in symptomatic hemodialysis patients? 939 20


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