Hidden in Plain Sight: An Unusual Cause of Rapidly Progressive Renal Failure.

Hyperoxaluria and resultant oxalate nephropathy are infrequently reported causes of irreversible renal failure. A rapid decline in renal function in an otherwise insidiously progressive oxalate nephropathy may be triggered by various superimposed insults like the use of nephrotoxic drugs. We present the case of a patient with rapidly progressive renal failure due to oxalate nephropathy that lead to a retrospective diagnosis of chronic pancreatitis. This case highlights the importance of timely assessment for enteric hyperoxaluria in patients with unexplained renal failure of tubulointerstitial nature.

Teenager male with burning pain in extremities--suspect Fabry disease, 2 case reports.

INTRODUCTION: We present 2 cases of teenager males presented with burning pain in extremities and turned out to be cases of Fabry disease.The purpose of presenting this case is to highlight the fact that suspicion of Fabry disease in patients presenting with these symptoms will lead to early diagnosis and treatment of this condition before occurrences of complications. CASE REPORT 1: A 14-year-old male presented with severe burning pain in both hands and feet since last 4 yrs which persisted despite consumption of painkillers and becoming more disabling and without having any family history for such condition. On general examination patient had small reddish coloured lesions around the umbilicus, appearing like angiokeratomas. Skin biopsy confirmed the lesion. On enzyme assay his alpha galactosidase activity found to be '0' nmol/hr/mg of protein, confirming his diagnosis. Patient's creatinine and 2 D ECHO were normal and urine had 1+ proteinuria. Patient started on carbamazepine tablets for pain and referred to higher centre for genetic diagnosis and enzyme replacement therapy. CASE REPORT 2: An 18-year-old male referred to our hospital by general practitioner for fatigue and pedal oedema with deranged renal function tests. On history taking patient gave history of severe burning pain in both hands and feet since age of 9 yrs. Patient's general examination revealed hypertension with pallor, pedal oedema along with angiokeratomas in bathing suit distribution. Patient's ultrasonography of kidney revealed bilaterally normal sized kidneys with altered echotexture and urine examination showed fine granular foamy cells with sub nephrotic range proteinuria. 2 D ECHO revealed concentric left ventricular hypertrophy. Skin biopsy report supported the diagnosis of Fabry disease. Patient advised to undergo renal biopsy to confirm Fabry nephropathy but patient denied any further diagnostic workup for nephropathy or Fabry disease. Patient started on conservative treatment and carbamazepine in renal dose given for acroparaesthesias. On discharge patient has been advised to visit higher centre for further diagnostic work up and enzyme replacement therapy. CONCLUSION: Suspicion of Fabry disease in teenager males presenting with symptoms of burning pain in extremities may lead to early diagnosis and treatment of this condition before occurrences of complications.

Chorea as a rare manifestation of hyperglycaemia.

INTRODUCTION: We present a case of chorea presenting as a clinical manifestation of hyperglycaemia.The purpose of presenting this case is to highlight the fact that movement disorder may be the clinical presentation of hyperglycaemia and it reverts on treatment of hyperglycaemia. CASE PRESENTATION: A 66-year-old female known case of type 2 diabetes mellitus and on oral hypoglycaemic drugs presented with abnormal and involuntary movements of the whole body and face since 7 days and high plasma glucose (446 mg/dl) and without ketosis. On controlling the blood sugar, there has been significant decrease in choreiform movements within 48 hrs and complete resolution of involuntary movements found at discharge at 1 week. CONCLUSION: Movement disorder like chorea may be the clinical presentation of the hyperglycaemia which could completely recover on rapid detection and correction of hyperglycaemia.

Clinical effectiveness of low-dose chlorthalidone (6.25 mg) + atenolol combination in stage I hypertensive patients: a multicenter, randomized, controlled study.

OBJECTIVE: To compare the efficacy and safety of low-dose chlorthalidone + atenolol combination with atenolol and atenolol + amlodipine combination in stage I hypertensive patients uncontrolled on active run-in monotherapy. METHODS: Newly diagnosed stage I hypertensive patients were randomized to active run-in monotherapy either with atenolol 25 mg (98/300) or chlorthalidone 6.25 mg (100/300) or amlodipine 2.5 mg (102/300). A total of 282/300 patients (atenolol 92, chlorthalidone 91, amlodipine 99) completed the active run-in phase successfully. Patients uncontrolled on active run-in monotherapy (atenolol 33, chlorthalidone 45, amlodipine 47) received the study treatment, namely atenolol 50 mg alone, chlorthalidone 6.25 mg+atenolol 25 mg and atenolol 25 mg+amlodipine 2.5 mg, respectively. Efficacy of the therapy was evaluated by BP measurement at weeks 12 and 20 post-therapy. RESULTS: Post-active run-in monotherapies, the study treatment groups showed a significant fall in mean SBP and DBP from baseline (p<0.05). The mean fall in SBP and DBP was comparable for study treatments (atenolol 50 mg, atenolol 25 mg+chlorthalidone 6.25 mg and atenolol 25 mg+amlodipine 2.5 mg) (p=0.337 for SBP and p=0.054 for DBP) at week 12 and (p=0.744 for SBP and p=0.855 for DBP) at week 20; also, the percentage of responders was comparable for the three study treatment groups (p=0.799) indicating that the low-dose chlorthalidone+atenolol combination is noninferior to the high-dose atenolol alone and atenolol+amlodipine combination. No serious laboratory/clinical adverse events were reported in this study. CONCLUSION: Chlorthalidone 6.25 mg in combination with atenolol 25 mg is effective and safe in stage I (JNC 7) essential hypertensive patients. This low dose of chlorthalidone could reduce dose-related concerns over metabolic adverse effects and may lead to wider usage of this proven antihypertensive agent in combination therapy.

Correlation of clinical and histopathological studies in classification of leprosy.

This paper presents a study of 100 cases of leprosy of different clinical types. These 100 cases included 26 TT, 3 BT, 7 BB, 2 BL and 62 LL. All were subjected to skin biopsy and were classified on the basis of histopathological changes. It was observed that there was some disagreement in clinical and histopathological classification. Thus histopathologically there were 20 TT, 9 BT, 7 BB, 6 BL and 58 LL. It appears that skin biopsy may be studied in all cases of leprosy. A combination of clinical features and histological changes in skin biopsy may help in better classification of leprosy.

A study of cell mediated immunity in leprosy.

This paper presents a review of 123 cases of leprosy of different clinical types as regards to their status of cellular immunity. These 123 cases included 41 fresh cases, 18 cases of reaction and 64 cases of leprosy taking antileprosy treatment. Out of 41 untreated cases only 11 turned up for follow up and their lymphoblastic transformation was repeated 4 to 6 months after initiating the treatment. It was observed that cell mediated immunity as expressed in terms of percentage of blast cells is definitely depressed in leprosy, most in LL and least in TT. There is a definite increase in the percentage of blast cells after taking antileprosy treatment. The rise in percentage of blast cells and hence cellular immunity is relatively more in patients treated with Lamprene as compared to those treated with DDS. Reactions also have impact over immunity in leprosy. Thus, most of the patients with ENL show higher values for blast percentage as compared to those with lepra reaction. It appears that serial lymphocyte cultures if done in all cases of leprosy undergoing treatment will help in assessment of individual progress.

A study of cell mediated immunity in leprosy

This paper presents a review of 123 cases of leprosy of different clinical types as regards to their status of cellular immunity. These 123 cases included 41 fresh cases, 18 cases of reaction and 64 cases of leprosy taking antileprosy treatment. Out of 41 untreated cases only 11 turned up for follow up and their lymphoblastic transformation was repeated 4 to 6 months after initiating the treatment. It was observed that cell mediated immunity as expressed in terms of percentage of blast cells is definitely depressed in leprosy, most in LL and least in TT. There is a definite increase in the percentage of blast cells after taking antileprosy treatment. The rise in percentage of blast cells and hence cellular immunity is relatively more in patients treated with Lamprene as compared to those treated with DDS. Reactions also have impact over immunity in leprosy. Thus, most of the patients with ENL show higher values for blast percentage as compared to those with lepra reaction. It appears that serial lymphocyte cultures if done in all cases of leprosy undergoing treatment will help in assessment of individual progress.