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

Laube, Guido F.; Sarkissian, Ashot; Hailemariam, Seife; Neuhaus, Thomas J.; Leumann, Ernst

doi:10.1007/s004310000684

Cited by 14 publications

(13 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The renal biopsy showed characteristic features of severe post-infectious glomerulonephritis (endocapillary proliferation, neutrophil infiltration, subepithelial humps, C3 deposits, and cellular crescents) and no thrombotic microangiopathy. HUS and PSGN can occur simultaneously [3]. However, our patient did not have laboratory or histological evidence of microangiopathy.…”

mentioning

confidence: 63%

Concomitant anuric post-streptococcal glomerulonephritis and autoimmune hemolytic anemia

2003

View full text Add to dashboard Cite

The association of acute renal failure (ARF) and severe anemia in children suggests the diagnosis of hemolyticuremic syndrome (HUS). We describe a child with anuric ARF and profound anemia secondary to a poststreptococcal glomerulonephritis (PSGN) and an autoimmune hemolytic anemia (AIHA).A 10-year-old African-American male was admitted because of ARF and acute anemia. One week before admission he had been prescribed amoxicillin for a streptococcal pharyngitis. Complete blood count at that time was normal (Hb 12.5 g/dl). Over the following 5 days he developed non-bloody diarrhea. At the local hospital, he was found to be severely anemic and in ARF: Hct was 7%, Hb was 2.7 g/dl, platelet count was 547,000/mm 3 and schistocytes were detected on a blood smear. BUN was 230 mg/dl and creatinine was 7 mg/dl. He received a packed red cell transfusion en route to our hospital. On admission at our hospital, repeat laboratory tests showed a BUN of 226 mg/dl, creatinine of 6.6 mg/dl, Hb of 5.5 g/dl, Hct of 15.5%, and a platelet count of 457,000/mm 3 . Repeat peripheral smear showed numerous spherocytes but no schistocytes. C3 was 20 mg/dl (reference range 83-154 mg/dl), C4 was 48 mg/dl (reference range 10-38 mg/dl), and anti-streptolysin O titers were 1440 IU/ml (normal <250 IU/ml). Antinuclear antibodies were negative. The patient was oliguric and white and red blood cell casts were observed on the urinalysis. A PSGN was suspected and confirmed later by renal biopsy. Further evaluation of the anemia showed that reticulocyte counts were 8.8% to 13.9%, LDH was 199 IU/l (reference range 60-160 IU/l) and haptoglobin was 270 mg/dl (reference range 13-163 mg/dl). A direct Coombs' test was positive, the direct IgG anti-globulin test (IgG-DAT) was negative, but DAT using anti-C3d reagent was positive. Cold agglutinins were negative. The final diagnoses were concomitant Donath-Landsteiner hemolytic anemia and PSGN. The patient received peritoneal dialysis for 8 days. The autoimmune hemolytic anemia was treated with prednisone (2 mg/kg per day) for 2 weeks and then tapered for 10 weeks. He responded well to prednisone and had a full renal and hematological recovery within 4 months. Two years later he is not anemic, his renal function remains normal, he is normotensive and has no proteinuria.In pediatric patients with ARF and severe hemolytic anemia, HUS is the most likely diagnosis. The fact that our patient had normal platelet counts and no schistocytes on the blood smear ruled out a classic HUS and its variants (Table 1) [4,5,7]. The renal biopsy showed characteristic features of severe post-infectious glomerulonephritis (endocapillary proliferation, neutrophil infiltration, subepithelial humps, C3 deposits, and cellular crescents) and no thrombotic microangiopathy. HUS and PSGN can occur simultaneously [3]. However, our patient did not have laboratory or histological evidence of microangiopathy. The severity of the anemia could not be easily explained by the PSGN: the anemia accompanying a PSGN is usually mild, secondary to hemodi...

show abstract

mentioning

confidence: 63%

Concomitant anuric post-streptococcal glomerulonephritis and autoimmune hemolytic anemia

2003

View full text Add to dashboard Cite

show abstract

“…[14] However, APIGN causing secondary malignant hypertension is described in handful of cases. [34567] Some of the cases described in literature do not have histological counterpart of TMA. However, they fulfilled clinical and biochemical criteria.…”

Section: Discussionmentioning

confidence: 99%

“…Neuraminidase antigen from streptococcal infection is said to produce endothelial injury and cause TMA. [34567] We report a case of APIGN with focal crescents associated with TMA secondary to malignant hypertension. Altered renal parameters were restored to normal after successful bllod pressure control and steroids therapy.…”

Section: Introductionmentioning

confidence: 99%

Atypical presentation of post infectious glomerulonephritis as malignant hypertension and thrombotic microangiopathy

et al. 2014

View full text Add to dashboard Cite

Infection-related glomerulonephritis presents commonly as acute nephritic illness, hypertension, hypocomplementinemia following an episode of pharyngitis or pyoderma. Atypical features like thrombotic microangiopathy (TMA), produced by neuraminidase antigen targeting endothelium have been described rarely. We report a case of TMA secondary to malignant hypertension, coexisting with post infectious glomerulonephritis.

show abstract

“…TTP is characterized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, fever, acute renal injury, and neurological abnormalities (Copelovitch & Kaplan, 2008). TMA has been reported in 8 patients with APSGN, consisting of 5 children and 3 adults (Duvic et al, 2000;Izumi, et al, 2005;Laube, et al, 2001;Medani et al, 1987;Proesmans, 1996;Siebels et al, 1995;Tan et al, 1998). All patients exhibited severe hypertension.…”

Section: Thrombotic Microangiopathymentioning

confidence: 99%

“…The precise pathogenesis of TMA in patients with APSGN is unclear, although two causes have been postulated: severe hypertension and streptococcal neuraminidase (Duvic et al, 2000;Laube et al, 2001;Izumi et al, 2005). HUS has been reported as a complication of severe hypertension, regardless of the cause (Broyer, 1995).…”

Section: Thrombotic Microangiopathymentioning

confidence: 99%

Atypical Clinical Manifestations of Acute Poststreptococcal Glomerulonephritis

Watanabe¹

2011

An Update on Glomerulopathies - Clinical and Treatment Aspects

View full text Add to dashboard Cite

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

Cited by 14 publications

References 12 publications

Concomitant anuric post-streptococcal glomerulonephritis and autoimmune hemolytic anemia

Concomitant anuric post-streptococcal glomerulonephritis and autoimmune hemolytic anemia

Atypical presentation of post infectious glomerulonephritis as malignant hypertension and thrombotic microangiopathy

Atypical Clinical Manifestations of Acute Poststreptococcal Glomerulonephritis

Contact Info

Product

Resources

About