Membranoproliferative glomerulonephritis in a carcinoma with unknown primary: an autopsy study

Kidney disease frequently complicates malignancy and its treatment. Although many solid and hematologic cancers may involve the renal parenchyma, clinical sequelae are usually not prominent. Published reports cite membranous nephropathy as the most common malignancy-associated glomerulopathy, occurring with many carcinomas and occasionally with leukemia and lymphoma followed by minimal change disease. Rarely membranoproliferative glomerulonephritis (MPGN) has been reported in patients with malignancy. The mechanism by which malignancy induces disease remains unproved, but may involve deposition of tumor antigen in the subepithelial space with in situ immune complex formation and subsequent complement activation. Treatment of the underlying malignancy may lead to resolution of nephrotic syndrome, lending indirect support to this theory. We report a rare autopsy case of a patient with metastatic carcinoma (with unknown primary) associated with MPGN. The association between MPGN and metastatic carcinoma with unknown primary is uncommon and has not been previously reported in the literature.     

New possibilities in the treatment of Meniere's disease

The results of the treatment of Meniere's disease by intratympanic instillation of gentamicin in 32 patients over a 24-months period were analyzed. The receded vestibular function was found in 96.8% patients, whereas in the remaining 3.2% pronounced vestibular hypofunction was observed. One month after the treatment vertiginous attacks disappeared in all the patients. However, three months after the treatment infrequent episodes of mild degree vertigo and mild unsteadiness that did not require additional intratympanic gentamicin application appeared in 15% of the patients with Meniere's disease. The vertiginous attacks ceased or were pronouncedly reduced in 85% of the patients. The unstable vestibular hypofunction was successfully converted into stabilized, centrally compensated areflexia. Intratympanic gentamicin exerted better results than the other invasive therapies for intractable Meniere's disease.     

Experience with similar biologic rituximab in 77 patients of granulomatosis with polyangiitis—a real-life experience

Clinical Rheumatology - To present single centre experience on the efficacy and safety of similar biologic of rituximab in patients with granulomatosis with polyangiitis (GPA). This was a...     

Seasonal influenza vaccination policies in the Eastern Mediterranean Region: Current status and the way forward

Background

The World Health Organization recommends annual influenza vaccination, especially in high-risk groups. Little is known about the adoption and implementation of influenza vaccination policies in the Eastern Mediterranean Region.

Successful renal transplantation in a family with a novel mutation in COL4A3 gene and autosomal recessive Alport syndrome

Alport syndrome (AS) is an inherited disorder of basement membranes caused by mutations affecting specific proteins of the type IV collagen family, presenting with nephropathy and extrarenal manifestations such as sensorineural deafness and ocular anomalies. Ten percentage to 15% of the patients with AS have autosomal recessive (ARAS) due to mutation in either COL4A3 or COL4A4 gene. We report a novel mutation in the COL4A3 gene in an Indian family with ARAS. The above‐mentioned genetic anomaly was a missense variation in exon 26 of the COL4A3 gene (chr2:228137797G>A; c.1891G>A) that resulted in the amino acid substitution of Arginine for Glycine at codon 631 (p.Gly631Arg) that was present in the heterozygous state in the asymptomatic parents and homozygous state in the male offspring who presented with early‐onset end‐stage renal disease, lenticonus and hearing loss. The patient (male offspring) underwent successful renal transplantation with his mother as a donor.     

Recognizing, Scoring, and Predicting Blast Injuries RID="" ID="" This International Association for the Surgery of Trauma and Surgical Intensive Care (IATSIC) article was presented at the 37th World Congress of Surgery International Surgical Week (ISW97), Acapulco, Mexico, August 24–30, 1997.

n = 665, 51%) had an ISS ranging from 0 to 34 (mean 13) had wounds ranging from G1ST (soft tissue wounds caused by low energy transfer) to G3VF (massive wounds with fractures and injury of vital structures) according to the RCWC, with PSS/IS scores from 2 to 105 (mean 60). Statistically significant correlation was found between ISS and PSS/IS as well as RCWC and PSS/IS. Cytokines (IL-1, TNF _alpha ) and amino acids responded to a blast injury in similar manner as to gunshot wounds with a greater ISS or more severe RCWC injury type. The subjective sensations in blasted patients (deafness, thoracic pain, vertigo) and mediators, confirmed in previous experimental investigations as important factors in the pathogenesis of blast injuries (TxA ₂ , sulfidopeptide leukotrienes) were relationed only to the PSS/IS.RID=" ID=" <E5>Correspondence to:</E5> I. Cernak, M.D., Ph.D.     

Assessment of four biochemical markers of bone metabolism in postmenopausal osteoporosis

In order to sudy the specificity and sensitivity of markers of bone metabolism in postmenopausal osteoporosis we investigated bone alkaline phosphatase, osteocalcin and carboxyl-terminal propeptide of procollagen type I in sera as markers of bone formation, and deoxypyridinoline in urine as a marker of bone resorption. The investigated parameters were determined in 53 women with confirmed osteoporosis and in a control group consisting of 45 healthy postmenopausal women without bone changes who were 40 to 79 years old. All biochemical markers were determined by monoclonal competitive enzyme immunoassay tests obtained by Metra Biosystems. The activity of bone alkaline phosphatase and the concentration of osteocalcin, procollagen type IVC-terminal propeptide (PICP), and deoxypyridinoline were grouped according to age of postmenopausal healthy and osteoporotic women. The values of all bone markers gradually increased with age, but significantly higher values were obtained in groups of postmenopausal osteoporotic women. By using receiver operator characteristic curve analysis, a very high specificity and sensitivity of the investigated biochemical markers in the diagnosis of postmenopausal osteoporosis were proven. The areas under the PICP curve and the osteocalcin curve were significantly higher than the area under the deoxypyridinoline curve, demonstrating a higher discriminating power of PICP and osteocalcin than deoxypyridinoline (p < 0.05).     

Defective fatty acid uptake modulates insulin responsiveness and metabolic responses to diet in CD36-null mice

Deficiency of the membrane protein FAT/CD36 causes a marked defect in fatty acid uptake by various tissues and is genetically linked to insulin resistance in rats and humans. Here, we examined insulin responsiveness of CD36-/- mice. When fed a diet high in complex carbohydrates and low (5%) in fat, these animals cleared glucose faster than the wild-type. In vivo, uptake of 2-fluorodeoxyglucose by muscle was increased severalfold, and in vitro, insulin responsiveness of glycogenesis by the soleus was enhanced. Null mice had lower glycogen levels in muscle and liver, lower muscle triglyceride levels, and increased liver triglyceride content--all findings consistent with increased insulin-sensitivity. However, when the chow diet was switched to one high in fructose, CD36-/- mice but not wild-type mice developed marked glucose intolerance, hyperinsulinemia, and decreased muscle glucose uptake. High-fat diets impaired glucose tolerance equally in both groups, although CD36 deficiency helped moderate insulin-responsive muscle glucose oxidation. In conclusion, CD36 deficiency enhances insulin responsiveness on a high-starch, low-fat diet. It predisposes to insulin resistance induced by high fructose and partially protects from that induced by high-fat diets. In humans, CD36 deficiency may be an important factor in the metabolic adaptation to diet and in susceptibility to some forms of diet-induced pathology.     

(-)-Epigallocatechin-3-gallate Modulates the Differential Expression of Survivin Splice Variants and Protects Spermatogenesis During Testicular Torsion

The anti-apoptotic effect of (-)-epigallocatechin-3-gallate (EGCG) during unilateral testicular torsion and detorsion (TT/D) was established in our previous study. In mice, the smallest inhibitor of apoptosis, survivin, is alternatively spliced into three variants, each suggested to have a unique function. Here, we assessed how EGCG exerts its protective effect through the expression of the different survivin splice variants and determined its effect on the morphology of the seminiferous tubules during TT/D. Three mouse groups were used: sham, TT/D+vehicle and TT/D treated with EGCG. The expression of the survivin variants (140 and 40) and other apoptosis genes (p53, Bax and Bcl-2) was measured with semi-quantitative RT-PCR. Histological analysis was performed to assess DNA fragmentation, damage to spermatogenesis and morphometric changes in the seminiferous tubules. In the TT/D+vehicle group, survivin 140 expression was markedly decreased, whereas survivin 40 expression was not significantly different. In parallel, there was an increase in the mRNA level of p53 and the Bax to Bcl-2 ratio in support of apoptosis induction. Histological analyses revealed increased DNA fragmentation and increased damage to spermatogenesis associated with decreased seminiferous tubular diameter and decreased germinal epithelial cell thickness in the TT/D+vehicle group. These changes were reversed to almost sham levels upon EGCG treatment. Our data indicate that EGCG protects the testis from TT/D-induced damage by protecting the morphology of the seminiferous tubules and modulating survivin 140 expression.