Tenofovir is an antiretroviral drug used in combination with other antiretroviral agents. It is an effective therapy for HIV infection. Kidney injury induced by this drug has been known to occur in the HIV positive patients. When given in titrated doses, it is safe and should be combined with regular monitoring of renal function and serum phosphate levels. We present a case report of Tenofovir induced nephropathy in a patient diagnosed to have acquired immunodeficiency syndrome 8 years ago and was on TDF based anti‑retroviral therapy. The patient had normal serum creatinine, normal blood glucose levels, raised serum bilirubin and amylase levels, mild anemia with glycosuria and proteinuria. Renal biopsy revealed normal glomeruli with dilated proximal tubules and attenuation of brush border. Our case reverted back to normal upon withdrawal of drug. We present this case to emphasize that the clinician should be aware of TDF induced acute kidney injury (AKI) presentation.
Background: Phosphorus is an essential nutrient required for multiple physiological functions, recent researches found that high phosphorus intake could have detrimental effects on health. Hyperphosphatemia is one of the most important risk factors for morbidity and mortality for chronic kidney disease (CKD) patients. High phosphorus intake can cause vascular and renal calcification, renal tubular injury, and premature death in multiple animal models. Limited data exist linking high phosphorus intake directly to adverse clinical outcomes. Small studies in human suggest that high phosphorus intake may result in positive phosphorus balance and correlate with renal calcification and albuminuria.Further prospective studies are needed to determine whether phosphorus intake is a modifiable risk factor for kidney disease.
Aims & Objectives: To study the effect of dietary habits on dietary phosphorous intake in chronic kidney disease patients on hemodialysis.
To study the prevalence of hyperphosphatemia in patients of CKD on maintenance hemodialysis.
To see the impact of dietary control of phosphorus in CKD patients.
This was a cross sectional comparative study. It was carrying in tertiary care centre in western region Maharashtra state.
A total of 80 patient’s diagnosed case of CKD on maintenance of hemodialysis were selected for the study, patients on maintenance hemodialysis program twice in a week with 4 hour duration.
Patients were divided into two groups as 1st group is on given diet to control phosphorus level in body and 2nd group is on phosphate binder to control phosphorus level.
Baseline serum phosphorus was measured 1 month before hemodialysis and after 1 month prior hemodialysis in both group patients.
Results: It was observed that there was a significance difference between the pre and post phosphorus of group A(experimental group). The main difference was seen between age group 20-40 and 40-60, no difference was seen in age group 60-80. There was significant difference in pre and post phosphorus was also seen in group B, in group B age group 60-80 has shown good response.
Conclusion: Renal diet education can reduce phosphorus level and guided diet education provides an additional benefit on controlling hyperphosphatemia in haemodiaylsis patient. The purpose of the study is to see the effect of dietary habits on dietary phosphorus intake in CKD Patients on haemodialysis. Dietary counseling encourage the consumption of foods with least amount of inorganic or absorbable serum phosphorus, low phosphorus- to –protein ratio an adequate protein content .Our phosphorus additives list helps to reduce indirectly intake of phosphorus. Younger group of patient have followed renal diet for hyperphosphatemia effectively.
This study investigated the histomorphological effect of mercury chloride on the kidney. Heavy metals are hazardous substances that cause serious health risk to ecosystems and organisms due to their high toxicity conferred by nature of their environmental persistence. Mercury is a well-known toxic heavy metal to animals as well as humans. Mercury occurs naturally in the environment in different chemical forms. Elemental mercury is the form used in dental amalgams. Forms more commonly found in nature are inorganic mercury and organic mercury. All mercury forms are considered toxic. It is being widely used in the industrial, medical, agriculture and other fields.
Materials and Methods: Thirty six (36) adult wistar rats of both sexes, weighing between 110 g-300 g were randomly divided into four groups A, B, C, and D with nine animals per group. The animals in groups B, C, and D were administered mercury chloride orally at the concentration of 0.2 mg/kg, 0.4mg and 0.5 mg/kg body weights respectively while group (A) served as control and was given distilled water. The administration lasted for a period of 21 days and on the 22nd day all the groups of rats were sacrificed by cervical dislocation, blood was collected through cardiac puncture and the kidneys were carefully removed and weighed immediately with a sensitive balance and then fixed in 10% formol saline. The tissues were processed and sectioned and stained with haematoxylin and eosin stain for histological studies. The results showed that the mean kidney weight in groups B and C increased insignificantly (P>0.05), compared to the control group while group D decreased significantly compared to the control group.
In the biochemical analysis there was significant increase (P<0.05).in alanine transaminase,, aspartate transaminase and alkaline phosphatase activities in mercury- treated group B, C and D compared to the control group A. Histological study of the kidney revealed that C and D treated groups showed marked degenerative changes, fibrosis and hemorrhage showing varying degrees of renal injury marked by focal sclerosis of the glomerulus, widening of the Bowman’s space and hyper cellularity and complete collapse of the glomerulus.
The study concluded that exposure to mercury chloride induced nephrotoxic effect on the kidney of adult wistar rats.
Background: Mineral bone disease in chronic kidney disease patients is associated with high morbidity and mortality, and it has been reported to start early in the course of the disease and worsen as the kidney damage progresses. However, the prevalence and factors associated with mineral bone disease in chronic kidney disease patients in our setting has not been established, so we aimed to determine the prevalence and factors associated with mineral bone disease among patients with chronic kidney disease at a tertiary Muhimbili National Hospital in Dar es salaam, Tanzania so as to help physicians recognize the patients at risk, diagnose the problem and prevent complications sooner.
Methods: This was a hospital based cross-sectional study involving adult patients with chronic kidney disease attending renal unit Muhimbili National Hospital, a tertiary referral center in Dar es Salaam, Tanzania. In this study, CKD-MBD was defined basing on the abnormality of serum calcium, phosphate or parathyroid hormone level. Data analysis was done using the SPSS version 23.0 software.
Results: A total of 300 participants with chronic kidney disease stage 3 and above were included in this study. Majority were male, 198 (66.0%), with a mean age of 53 years. The prevalence of mineral bone disease was found to be 75.0%. The most common form of mineral bone disease was hyperparathyroidism 196 (87.1%), followed by hypocalcemia 174 (77.3%) and hyperphosphatemia 82 (36.4%), which was the least common.
Factors which were found to be significantly associated with CKD-MBD were the use of calcium supplements, use of phosphate binders, being on dialysis, a calcium rich diet and a low phosphate diet.
Conclusion: Mineral bone diseases are common in patients with CKD at Muhimbili National Hospital. Patients with CKD should undergo serial assessment of phosphate, calcium and parathyroid hormone level, considered together, so as to diagnose mineral bone disease early and treat those patients who will be found to have persistently or prolonged abnormalities in these bone mineral biomarkers.
The importance of hyperglycaemia without glycosuria, seems to have been under played, as evidenced by the paucity of reports about the same, in the literature. Ralph H. Major et al.  observed in JAMA, on review of literature till then, that there was no reported case as such, in the literature before. CF. Davidson et al.  reported in the Journal of Endocrinology, that between 1932 t0 1937 inclusive, not even a single case of hyperglycaemia without glycosuria was reported in the literature. Hardly there are not even a handful of cases reported till this date, as observed by this author. The awareness appears to be low, as regards to the significance of this syndrome. With the dispensing off, of urine glucose testing, consequent to the advent of home monitoring of the blood sugar with glucometer, there is a every chance of missing this entity. The complacency, that this is just as sequel to the increased renal threshold /tubular maximum that occurs in the natural history of long standing DM2, could also be contributory for not taking this syndrome seriously. This fatalistic attitude, might under score the underlying structural and functional damage of the kidneys. This article aims to shift the emphasis to renal glomerular than tubular pathology, leading to the syndrome of hyperglycaemia without glycosuria.DM2, being the leading cause of the end stage renal disease (ESRD),focus on this syndrome is expected to create awareness among the patients of DM2,about the underlying serious structural and functional damage, to their kidneys. This syndrome is hoped to serve as a biomarker of DKD (diabetic kidney disease) progressing to ESRD, which helps the diabetic patient to seek nephrologist's consultation/ intervention earlier than otherwise. It could serve as a prelude for ordering other tests like estimated glomerular filtration rate (eGFR) and protein –creatinine (PCR) ratio etc. The necessary pathophysiological basis is provided for proper understanding of this syndrome along with review of literature and emphasis on its importance in the early recognition and prevention of ESRD, are focussed in this article.