International Journal of Urology and Nephrology

International Journal of Urology and Nephrology ISSN 2091-1254 Vol. 6 (6), pp. 001-005, June, 2018. © International Scholars Journals

Full Length Research paper

Causes and renal morphological changes in chronic renal failure: A retrospective study of 50 autopsy cases

Martin A Nzegwu¹*, J.U. Aligbe² and Femi Ogunbiyi³

¹Department of Anatomic Pathology University of Nigeria Teaching Hospital Enugu (UNTH). Nigeria.

²Department of Morbid Anatomy University of Benin Teaching Hospital,

³University College Hospital, Ibadan, Nigeria.

Accepted 12 April 2018

Abstract

The paper aims to determine the age and sex distribution of patients with end stage renal disease in Benin City, Nigeria, to study renal changes in chronic renal failure and determine where possible the causal/associated aetiopathologic agents in relation to chronic renal failure, and to compare results with those of similar studies done in other parts of the country. Complete autopsy was carried out on bodies of 50 patients who died of chronic renal failure at the University of Benin Teaching Hospital Benin City, after securing informed consent from the relatives. The kidneys were measured, weighed and described. In addition tissue samples were taken for histology using haematoxylin and eosin stain and the slides were subsequently read. Periodic acid Schiff and Masson’s Trichrome stains were applied to kidneys to address unresolved cases. All cases of acute renal failure due to shock were excluded from the study. As an inclusive criterion all cases used for the study were confirmed chronic renal failure patients who had been on dialysis for at least a period of 6 months and they all had a renal biopsy with histological confirmation of the type of renal lesions involved. Ethical approval was sought and granted by relevant authorities in UBTH before the study commenced in 2004. Twenty nine of the patients (58%) are males, 21 (42%) are females, with a male to female ratio of 1.38:1. The largest concentration of chronic renal failure (CRF) related deaths occurred in the 30- 39 years 18 (36%), with the age range varying from 8 years in a male child who died of Good Pastures syndrome, to a 65 year old woman dying of chronic hypertensive renal disease. The average age of patients dying CRF is 43.9 years SD 6.6. Adult polycystic kidney disease is responsible for 2 deaths (4%), Systemic lupus erythematosus one death (2%). Chronic glomerulonephritis is responsible for 21 deaths (42%), the most significant cause of both end stage kidney disease and CRF. Diabetic nephropathy is responsible for 7 deaths (14%); hypertension is responsible for 15 cases (30%). Chronic renal failure related deaths in Benin City have a slight male preponderance of 1.38:1, and occurred in the average age group of 43.9 years SD 6.6. The commonest causes here include chronic glomerulonephritis accounting for 42%; hypertension, 30% and Diabetic Mellitus, 14% of cases.

Key words: Chronic renal failure, changes, autopsy, retrospective study.

Key words: UTI, bacteria, antibiotic susceptibility.

International Journal of Urology and Nephrology ISSN 2091-1254 Vol. 6 (4), pp. 001-002, April, 2018. © International Scholars Journals

Case Report

Waldenström’s macroglobulinemia and cerebral lymphoplasmocytic proliferation: Bing-Neel syndrome

I. Tazi

Department of Medicine, Hematology Unit, Centre Hospitalier Régional Béni-Mellal Morocco or Hematology and paediatric Oncology Department, Hospital 20 Aout 1953, Casablanca, Morocco. E-mail: [email protected].

International Journal of Urology and Nephrology ISSN 2091-1254 Vol. 6 (4), pp. 001-009, April, 2018. © International Scholars Journals

Full Length Research Paper

Cysteamine in 3- nitropropionic acid model of Huntington’s disease in rats: Modulation of mitochondrial function and amino acid pattern

Hanan M. Abd El Gawad^1*, Hanan S. El-Abhar² and Nadia M. S. Arafa³

¹Biochemistry Department, Faculty of Pharmacy, Cairo University, Cairo, Egypt.

²Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.

³Physiology Department, National Organization for Drug Control and Research (NODCAR), Giza, Egypt.

Accepted 08 January, 2018

Abstract

Huntington disease (HD), a neurodegenerative disorder, is characterized by selective atrophy and cell loss within the striatum. 3-nitropropionic acid (3-NP) is a mitochondrial toxin that induces experimental HD-like disorders. Currently, although there is no treatment that can prevent the striatal neuropathology, cysteamine is considered one of the most promising candidate drugs for HD. Previous studies showed that cysteamine modulates 3- NP-induced HD, via several mechanisms; however, its effect on amino-acids profile and mitochondrial function was not tested before, which is the main aim of the current study. Male Wistar albino rats (200-250 g) were injected subcutaneously by 3-NP (20 mg/ kg/ day for 7 days), to serve as positive control group. Another group received cysteamine intraperitonealy in a building dose from 25 up to 75 mg/kg/day for 7 days, one hour before 3-NP. Normal untreated rats were used as negative control. The striatal biochemical parameters and serum amino acid pattern were assessed one hour after the last 3-NP injection. The mitochondrial toxin resulted in significant decrease in striatal citrate synthase (CS), creatine kinase (CK) and glutathione (GSH) accompanied by a marked increase in nitric oxide (NO) activity/ content. Significant reduction in branched chain amino acids, glycine, alanine, serine, taurine, tyrosine and histidine was also demonstrated in 3-NP- treated rats. Cysteamine administration markedly improved the mitochondrial function as exhibited by restoration of CS activity; however, no effect was noticed on the rest of the striatal biochemical parameters. In addition, some of the amino acids altered by 3-NP were ameliorated by cysteamine. In conclusion, results of the present study explored the importance of amino acid pattern in the pathogenesis of HD and confirmed the neuroprotective efficacy of cysteamine against HD which may be related at least partly, to its influence on amino acid metabolism and enhancement of mitochondrial function.

Key words: Huntington disease, cysteamine, oxidative stress, mitochondria, amino acids.