Influenza vaccination induced leukocytoclastic vasculitis and pauci-immune crescentic glomerulonephritis.

Influenza vaccination is a widely accepted practice, particularly among the elderly and high-risk individuals. Minor and transitory side effects following the vaccination are common, while systemic complications are infrequently reported. We describe here a case of a patient who presented to the emergency room with arthralgia, myalgias and purpura, following influenza vaccination. Necrotizing vasculitis associated with pauci-immune glomerulonephritis was observed on kidney biopsy. With increasing use of influenza vaccination, attention should be drawn to the possible expression of systemic adverse effects such as vasculitis and glomerulonephritis.

The effect of secondary hyperparathyroidism and hemodialysis therapy on alveolar bone and periodontium.

BACKGROUND: Alveolar bone is particularly sensitive to increased levels of parathyroid hormone (PTH) from either primary or secondary hyperparathyroidism (HPT). The purpose of this study was to examine the effect of secondary HPT on the periodontium of patients on hemodialysis. METHODS: The experimental group consisted of 35 patients with secondary HPT, with chronic renal failure treated by hemodialysis (E group). A control group (C group) was formed from 35 healthy age- and gender-matched subjects attending the maxillofacial outpatient clinic for a variety of reasons. Blood samples were taken from the E group, and the biologically active intact parathormone molecule, PTH(1-84), was assayed using two-site immunoradiometric assay (IRMA). The time of onset and the duration since diagnosis of HPT was also recorded. In addition, for a subgroup of 25 matched pairs of patients, a clinical periodontal examination was performed, and the Ramfjord index teeth were recorded for: Plaque index (PI); Gingival index (GI); Probing depth (PD); and Clinical attachment level (CAL). A standardized panoramic X-ray was taken from all patients and computer-based linear measurements were used to assess alveolar bone loss (BL). Unpaired Student's t-test served to compare the two groups. Pearson's correlation coefficient test was used to study the association between PI, PTH level, disease duration and BL. RESULTS: Demographically, both groups were similar with no statistical difference. PI was also similar in the C and E group (2.03 +/- 0.13 and 1.76 +/- 0.17, respectively). GI, however, was slightly greater in the C group (1.28 +/- 0.09) compared to the E group (0.97 +/- 0.01). PD in the E group (2.92 +/- 0.14 mm) was almost identical to that of the C group (2.90 +/- 0.12 mm). Likewise, CAL in the E group (4.43 +/- 0.29 mm) did not differ from CAL in the C group (4.03 +/- 0.25 mm). Mean BL was also similar in the E and C groups (3.60 +/- 0.23 mm and 3.85 +/- 0.24 mm, respectively). PI showed a positive, significant correlation with BL (r = 0.457, P = 0.0008). CONCLUSION: From this study it can be concluded that secondary HPT does not have an appreciable effect on periodontal indices and radiographic bone height.

Acute symptomatic hyponatremia complicating invasive cardiac procedures: a report of three patients.

Hyponatremic encephalopathy is a well-known complication of surgical procedures. This syndrome has not been described in the cardiology literature. We report three patients who developed acute hyponatremia with life-threatening encephalopathy following an invasive cardiac procedure. Diagnosis and treatment were delayed because of a lack of awareness for the syndrome among the cardiology staff. The diagnosis of hyponatremia should be suspected in any patient who develops behavioral or neurological manifestations following an invasive cardiac procedure. Prompt diagnosis and treatment are essential to avoid permanent neurological damage or death.

Renovascular hypertension associated with neurofibromatosis: two cases and review of the literature.

The authors report two cases of renovascular hypertension associated with neurofibromatosis. A 19-year-old woman was admitted to our hospital with a complaint of abdominal pain and blood pressure of 180/120 mmHg. Examination revealed café-au-lait spots over her chest and extremities. Peripheral plasma renin activity (PRA) under basal conditions was 2.8 ng/ml/h and increased to 12.6 ng/ml/h after administration of 50 mg captopril. Plasma and urinary catecholamines were normal. Selective renal angiography showed left aneurysmal dilatation of the segmentary branch and right renal artery stenosis with multiple aneurysmal affecting different branches. Blood pressure was controlled by multiple drugs, including beta-blockers and angiotensin-converting enzyme inhibitor. Another patient, a 20-year-old woman, was admitted because of severe arterial hypertension, numerous café-au-lait spots, scoliosis, and mass over the right arm. PRA from the right renal vein was extremely elevated, and selective angiography demonstrated bilateral renal artery stenosis. Aortorenal bypass was performed successfully.

Haptoglobin phenotype and diabetic nephropathy.

AIMS/HYPOTHESIS: To determine if the haptoglobin 2 allele is associated with an increased risk for the development of diabetic nephropathy. METHODS: This study included 110 consecutive normotensive subjects with Type I (insulin-dependent) diabetes mellitus and Type II (non-insulin-dependent) diabetes mellitus seen in two outpatient clinics in Israel. Diabetes duration was greater than 10 years for Type I diabetes and more than 5 years for Type II diabetic subjects. Microalbuminuria was defined as urinary protein excretion of 30 to 300 mg/24 h, and macroalbuminuria was defined as urinary protein excretion of greater than 300 mg/24 h. Serum was taken from subjects for haptoglobin typing by gel electrophoresis. RESULTS: Of the participating subjects 54 had Type I and 56 had Type II diabetes. None (0/18) of the subjects homozygous for the haptoglobin 1 allele (1-1) showed any sign of diabetic nephropathy, as compared with 34 % (19/55) of subjects homozygous for the haptoglobin 2 allele (2-2) and 27 % (10/37) of heterozygous subjects (2-1) (p < 0.04). Of the subjects 29 showed macroalbuminuria. The risk of developing macroalbuminuria was found to be greater in subjects with two haptoglobin 2 alleles (22 %) (12/55) as compared with one haptoglobin 2 allele (8 %) (3/37) or no haptoglobin 2 alleles (0%) (0/18) (p < 0.03). CONCLUSION/INTERPRETATION: By showing a graded risk relation to the number of haptoglobin 2 alleles in Type I and Type II diabetic subjects, these studies further support our hypothesis that the haptoglobin phenotype is a major susceptibility gene for the development of diabetic nephropathy.

Hypoxic induction of vascular endothelial growth factor is markedly decreased in diabetic individuals who do not develop retinopathy.

OBJECTIVE: A small percentage of patients do not develop any evidence of diabetic retinopathy (DR) even after many years of diabetes. Vascular endothelial growth factor (VEGF) has been implicated in the development of DR. Therefore, we sought to determine if the regulation of VEGF differs in those patients who develop DR after many years of diabetes compared with those who do not develop DR. RESEARCH DESIGN AND METHODS: We performed standard 7-field stereoscopic fundus photography on 95 consecutive patients with type 1 and type 2 diabetes. Patients were categorized into 3 groups according to the presence or absence of DR and the duration of diabetes: group 1 was defined by presence of DR, group 2 was defined by absence of DR after >10 years duration of diabetes, and group 3 was defined by absence of DR with long-standing diabetes (> or =20 years for type 1 diabetes and > or =15 years for type 2 diabetes). Monocytes from 40 ml peripheral blood were isolated from all patients, and the hypoxic induction of VEGF was determined in vitro. RESULTS: We found no significant difference in the basal level of VEGF in patients with and without DR. However, we did find a markedly significant difference in the hypoxic induction of VEGF between patients from group 1 and group 3 (4.35+/-0.55 vs. 1.87+/-0.3, P<0.00013). CONCLUSIONS: This study suggests that 1 mechanism for the absence of DR in patients with long-standing diabetes is a decreased hypoxic induction of VEGF.

Developmental change in Na,K-ATPase alpha1 and beta1 expression in normal and hypothyroid rat renal cortex.

Renal Na,K-ATPase drives active reabsorption of sodium and cotransported solutes along the nephron. There is a large increase in net Na(+) reabsorption in the postnatal rat kidney. It has previously been established that the postnatal increase in expression of sodium pump isoforms in the brain, but not the heart, is blunted in the hypothyroid neonate. The aims of this study were to establish whether the developmental increase in renal sodium transport is associated with coordinate increases in the abundance of the sodium pump alpha(1) catalytic and beta(1) glycoprotein subunits and Na,K-ATPase activity, and to determine whether thyroid status influences the postnatal increase in renal Na,K-ATPase expression. Pregnant rats were made hypothyroid with low iodine diet, propylthiouracil and perchlorate. Offspring were hypothyroid assessed by triiodothyronine/thyroxine RIA. Renal cortical membranes were prepared from euthyroid and hypothyroid rats from 6 to 24 days of age. There was no change in Na,K-ATPase activity or expression between 6 and 15 days. Between 15 and 24 days, Na,K-ATPase activity increased 1.35-fold while sodium pump alpha(1) and beta(1) subunit abundance increased coordinately to 1.7- and 2-fold over the previous period, respectively. In hypothyroid neonates, kidney weight was less than in euthyroids, and Na,K-ATPase activity, alpha(1) and beta(1) subunit pool sizes did not significantly increase as a function of age between 6 and 24 days. We conclude that the postnatal increase in sodium pump activity can be accounted for by coordinate increases in the pool sizes of alpha(1) and beta(1) subunits and that, like in brain, this increased Na,K-ATPase expression is dependent on normal thyroid status.

Minimal change glomerulonephritis associated with hydatid disease.

A 63-year-old man presented to our department with dyspnea and peripheral edema. A cystic mass in the right upper abdomen, consistent with echinococcal disease was discovered. Proteinuria was also present, and a nephrotic syndrome was diagnosed. The kidney biopsy revealed minimal change glomerulonephritis. Treatment with the antiechinococcal drug albendazole induced complete remission of the nephrotic syndrome, suggesting an etiopathogenic role for a hydatid antigen in the development of an immune-mediated glomerulonephritis.

Acute oliguric renal failure associated with unilateral renal embolism: a successful treatment with iloprost.

A 66-year-old woman presented with acute-onset rapid atrial fibrillation and right upper quadrant pain which had appeared 24 h prior to admission. The patient also manifested acute oliguric renal failure (serum creatinine 6.9 mg/dl). Selective renal angiography revealed total occlusion of the right renal artery with normal visualization of the left kidney vasculature. The patient was treated with intra-arterial urokinase and intravenous heparin, with no response. Intravenous administration of the prostacyclin analogue, iloprost, resulted in rapid resolution (within hours) of the oliguric acute renal failure, in spite of the continuing presence of a nonfunctioning right kidney. We conclude that the etiology of the acute renal insult in this patient is probably related to unilateral renal arterial embolization accompanied by arterial spasm of the unaffected kidney. The contralateral vasospasm can be reversed by iloprost, which then leads to a rapid recovery from acute renal failure. We are unaware of prior reports documenting the beneficial effect of iloprost in a clinical setting as described here.

Minimal-change nephropathy and malignant thymoma.

A 69-year-old woman presented with persistent dyspnea and continuous coughing and mediastinal mass. The mass was found to be a malignant thymoma and was resected incompletely. A full-blown nephrotic syndrome appeared 1 year after removal of the thymoma. Renal biopsy revealed minimal-change glomerulonephritis. There was no evidence of other autoimmune diseases or causes of the minimal-change glomerulonephritis.

Complete adaptation to chronic potassium loading after adrenalectomy: possible humoral mechanisms.

This study was designed to evaluate the mechanisms of adaptation to chronic potassium loading after bilateral adrenalectomy. Studies were performed in Sprague-Dawley rats subjected to 3 days of normal diet and 9 days of high KCl diet followed by adrenalectomy or sham operation on the thirteenth day and 9 additional days of potassium loading (groups 1 and 2, respectively). Animals that underwent adrenalectomy and intact animals, both receiving a normal diet, served as the control groups (groups 3 and 4, respectively). Plasma potassium, urinary potassium and sodium excretion rates, plasma aldosterone and insulin, and Na+-K+ ATPase activity in renal cortical and medullary homogenates were measured. Within 5 days of adrenalectomy the urinary potassium excretion rate in potassium-loaded rats that underwent adrenalectomy (group 1) reached the level observed in potassium-loaded intact rats (group 2), but a significant elevation in plasma potassium levels among rats in group 1 was noticed. In both of the potassium-loaded groups plasma insulin levels and renal cortical and medullary Na+-K+ ATPase activity were significantly higher compared with those in respective control groups receiving a normal diet. Acute clearance experiments carried out in adrenalectomized rats infusing the sera of the potassium-adapted rats that underwent adrenalectomy (obtained at the end of the chronic experiment) showed an uprise in urinary potassium excretion. This result was not observed after the infusion of control sera. These findings suggest that full renal adaptation to chronic potassium loading can be achieved in the absence of aldosterone through mechanisms that might be related to elevated plasma insulin levels (extrarenal); also, a humoral factor associated with the renal adaptation cannot be ruled out.

Effects of cyclosporin A on the synthesis, excretion, and metabolism of endothelin in the rat.

Increasing evidence suggests that endothelin, a potent vasoconstrictor, is implicated in cyclosporin A (CsA)-induced nephrotoxicity. Increased levels of urinary and circulating endothelin have been described in CsA-treated humans and animals. The exact mechanisms by which CsA induces these increases are still unknown, and no data indicate whether these elevated levels reflect increased synthesis or decreased clearance of endothelin. In the present study, we investigated the effects of CsA administration (50 mg/kg per day i.p. for 6 days) to rats on plasma and urinary levels of endothelin; expression of endothelin-1 (ET-1), ET-3, and endothelin-converting enzyme in renal tissue; clearance of infused 125I-ET-1; and degradation of 125I-ET-1 by recombinant neutral endopeptidase. Rats given CsA for 6 days developed severe renal insufficiency, as shown by a 74% decrease in creatinine clearance rate (Ccr) (P < .006). Ccr was remarkably improved in CsA-treated rats that received bosentan, the combined antagonist of both endothelin A and endothelin B receptors. Urinary excretion of endothelin increased from an undetectable level to 31.7 +/- 6.0 pg/24 h (P < .001), and plasma levels of endothelin were unchanged (2.8 +/- 0.2 to 3.1 +/- 0.2 pg/mL). Reverse transcription followed by quantitative polymerase chain reaction revealed that ET-1 mRNA in the renal medulla increased by 59% (P < .006), whereas the expression of both ET-3 and endothelin-converting enzyme was unchanged. In other rats, neither acute nor chronic treatment with CsA affected either the clearance of 125I-ET-1 from the blood or the renal and pulmonary uptake of the peptide. Moreover, CsA did not affect the degradation of 125I-ET-1 by highly purified recombinant neutral endopeptidase, a well-known endothelinase. Taken together, these data suggest that the elevated urinary endothelin levels obtained after CsA treatment originate from the kidney and reflect increased renal synthesis of ET-1. Moreover, the production of endothelin appears to be regulated at the mRNA transcription level, and expressions of ET-1 and ET-3 are regulated independently.