A boy with acute renal failure

Proesmans, Willem; Baten, Evert; Damme, B Van

doi:10.1007/bf02254224

Cited by 11 publications

(16 citation statements)

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“…The renal biopsy showed unequivocal lesions of acute glomerulonephritis and none of the characteristics of thrombotic microangiopathy. Again, hypertension was quite pronounced, as in our patient presented in "a case for diagnosis" [1]. We feel that these patients' features are compatible with -as stated by Broyer [2] -"mild, transient microangiopathic haemolytic anaemia as a consequence of severe hypertension related to acute glomerulonephritis".…”

supporting

confidence: 85%

“…About the time we submitted our second "A case for diagnosis" on a boy with acute renal failure [1], a 7-year-old girl was admitted to our renal unit with almost identical findings of acute renal failure with characteristics of both the haemolytic uremic syndrome (HUS) and acute glomerulonephritis. The child was born prematurely with a gestational age of 33 weeks.…”

Section: Sirsmentioning

confidence: 99%

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Haemolytic uraemic syndrome superimposed on acute glomerulonephritis

Proesmans

1996

Pediatr Nephrol

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About the time we submitted our second "A case for diagnosis" on a boy with acute renal failure [1], a 7-year-old girl was admitted to our renal unit with almost identical findings of acute renal failure with characteristics of both the haemolytic uremic syndrome (HUS) and acute glomerulonephritis. The child was born prematurely with a gestational age of 33 weeks. She stayed in the neonatology unit for 4 weeks. Her psychomotor development was mildly retarded and from the age of 3 years she had epilepsy which was first treated with sodium valproate and later carbamazepine. At the time of her acute renal failure she had been on carbamazepine only tbr about 1 year.After 5 days of loose stools, she was admitted to another hospital, mainly because of marked oedema. She was pale, had facial and pretibial oedema and a blood pressure of 110/70 mmHg (95th percentile). Her serum creatinine was 3 mg/dl and urea 360 mg/dl. She was oliguric and urine microscopy showed too numerous to count red blood cells (RBC) and 3+ proteinuria. The peripheral blood count showed a haemoglobin of 11.2 g/dl, 12,800 white blood cells (WBC) and 222,000 platelets/gl. She was prescribed bed rest, sodium restriction and frusemide. Over the next 5 days her haemoglobin dropped to 8.2 g/dl and platelets to 95,000/gl; urine output and serum creatinine improved, but her blood pressure rose to 164/96 mmHg. She was referred to us for diagnostic investigation.We saw an ill-looking, pale girl with eyelid oedema, no skin lesions, normal tonsils and a blood pressure of 160/ 120 mmHg. She had macroscopic haematuria with a urine output of 558 ml/24 h which contained 440 mg of protein.Her haemoglobin was 10 g/dl, WBC count 14,800 and platelets 192,000/pA. Serum haptoglobin was 0.14 g/1 (normal value 1-3 g/l). Serum electrolytes were unremarkable, creatinine was 1.7 mg/dl and urea 96 mg/dl. Creatinine clearance was 36 ml/min per 1.73 m 2. Plasma renin activity was 1.09 ng/ml per hour (normal value fo age 1-5). Serum protein electrophoresis showed a lowish albumin of 3.5 g/dl but elevated gammaglobulins of 1.66 g/ dl. Total complement was less than 100 U/ml (normal value 300-500 U/ml) with normal values for Clq, C3 and C4. The antistreptolysin (ASLO) titre was 1,180 IU/ml (normal value <200). Throat culture was negative for beta-haemolytic streptococci. Renal ultrasound showed two normalsized kidneys with a hyperechogenic cortex. With acombination of atenolol, nifedipine and enalapril, her blood pressure normalised progressively.A renal biopsy was performed. Light microscopy showed eight glomeruli with diffuse mesangial proliferation with a circumferential crescent in two. Tubuli and vessels were unremarkable, the interstitium was somewhat oedematous. On immunofluorescence (10 glomeruli), only C3 could be identified in a subendothelial position.At discharge 2 weeks later her blood pressure was 96/ 50 mmHg and serum creatinine 1.1 mg/dl. The urine had 1,500 RBC/gl by direct counting and proteinuria was only 40 mg/24 h. She was investigated again 6 months later, wh...

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supporting

confidence: 85%

Section: Sirsmentioning

confidence: 99%

Haemolytic uraemic syndrome superimposed on acute glomerulonephritis

Proesmans

1996

Pediatr Nephrol

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“…It has been speculated that these lesions might be secondary to severe hypertension, not observed in our patients [1,10,11]. Other authors postulated a common pathway whereby an unknown microorganism would cause complement consumption, endothelial dysfunction and micro-angiopathy [13].…”

Section: Discussionmentioning

confidence: 56%

“…The outcome was good in all patients, as expected in APGN in contrast to D-HUS. In two of them (patients 3 and 4), HUS was also con®ned to the haematological ®ndings, and renal biopsy showed only features of APGN [8,11]. Histology in the two other patients (patients 5 and 6), was consistent with both HUS and APGN [2,15].…”

Section: Discussionmentioning

confidence: 92%

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Simultaneous occurrence of the haemolytic uraemic syndrome and acute post-infectious glomerulonephritis

Laube¹,

Sarkissian

Hailemariam

et al. 2001

European Journal of Pediatrics

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We report on two children, a 12-year-old boy and a 6-year-old girl, with simultaneous occurrence of clinical and laboratory features consistent with both diarrhoea-negative haemolytic uraemic syndrome (D-HUS) and acute post-infectious glomerulonephritis (APGN). Both presented with acute renal insufficiency, hypertension and oedema. Laboratory evaluation revealed micro-angiopathic anaemia with burr cells, thrombocytopenia, elevated lactic dehydrogenase and low complement C3. Urinalysis showed marked proteinuria and haematuria. Renal biopsy was characteristic of APGN, but not of HUS. The outcome was good in both children. Conclusion. The simultaneous occurrence of diarrhoea-negative haemolytic uraemic syndrome and acute post-infectious glomerulonephritis is rare. The outcome is generally good as is expected in the latter condition in contrast to the former.

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Identification of the oxidation products of cysteamine and cystamine byCE‐MSinterfaced by a noncommercial electrospray ionization source

Carvalho

El-Attug

Silva

et al. 2012

J of Separation Science

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Sodium cysteamine phosphate is a prodrug derivative of cysteamine that can be used in cystinosis treatment. Although titrimetric assays are very well established and precise, iodimetric determination of sodium cysteamine phosphate requires considerably more carefulness and time from the analyst than usual. The possibility to assess sodium cysteamine phosphate by CE was evaluated by means of the quantification of its oxidation product, cystamine, which is a more suitable substance to be used as primary standard than sodium cysteamine phosphate. Apparently, this approach should be straightforward, but systematic differences between the results obtained with CE and titrimetric assays were noticed. MS and CE-MS were employed to aid in the investigation of the possible causes of imprecision of the sodium cysteamine phosphate titration and CE determination. For this purpose, a simple and inexpensive ESI source was constructed. It was observed that cystamine is not the final product of the cysteamine and/or sodium cysteamine phosphate iodine-oxidation and other species besides cystamine may be formed depending on the reaction conditions, which explains the difficulties observed in the sodium cysteamine phosphate quantification.

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A boy with acute renal failure

Cited by 11 publications

References 3 publications

Haemolytic uraemic syndrome superimposed on acute glomerulonephritis

Haemolytic uraemic syndrome superimposed on acute glomerulonephritis

Simultaneous occurrence of the haemolytic uraemic syndrome and acute post-infectious glomerulonephritis

Identification of the oxidation products of cysteamine and cystamine byCE‐MSinterfaced by a noncommercial electrospray ionization source

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