Hemolytic uremic syndrome complicated by Clostridium septicum bacteremia and new-onset type 1 diabetes mellitus. Report of a case

Iddings, Anna C; Shenoi, Asha; Pozzo, Alba Morales; Kiessling, Stefan G.

doi:10.5414/cn109049

Cited by 5 publications

(4 citation statements)

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“…An onset of complement deficiency, pneumococcal infection, abnormal metabolism of cobalamin, and so on can lead to atypical hemolytic uremic syndrome (aHUS), which is related to genetic mutations and has a distinct pathophysiology. [ 3 , 6 , 7 ] So far, only a few cases of HUS have been triggered by a metabolic disease, such as diabetes mellitus [ 8 , 9 ] and metabolic disorder of cobalamin. [ 10 , 11 ] Recently, Adrovic et al described a case of a 6-year-old girl with CblC disorder, who was found to have a homozygous mutation in exon 4 of MMACHC, c. 484G >T. [ 11 ] Although the serum level of VitB12 was normal in the patient, the bone marrow showed an obvious degeneration, so we highly suspected that it was caused by metabolic abnormalities of cobalamin.…”

Section: Discussionmentioning

confidence: 99%

Atypical hemolytic uremic syndrome induced by CblC subtype of methylmalonic academia

et al. 2017

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Rationale:Methylmalonic acidemia (MMA) is a common organic acidemia, mainly due to methylmalonyl-CoA mutase (MCM) or its coenzyme cobalamin (VitB12) metabolic disorders. Cobalamin C (CblC) type is the most frequent inborn error of cobalamin metabolism; it can develop symptoms in childhood and often combine multisystem damage, which leads to methylmalonic acid, propionic acid, methyl citrate, and other metabolites abnormal accumulation, causing nerve, liver, kidney, bone marrow, and other organ damage.Patient concerns:A 4-year-old girl presented with paleness, fatigue, severe normochromic anemia, and acute kidney injury.Diagnosis:Based on severe normochromic anemia and acute kidney injury, renal biopsy showed membranous proliferative glomerular lesions and thrombotic microvascular disease, supporting the diagnosis of aHUS. Although the serum vitamin B12 was normal, further investigation found the concentration of urinary methylmalonic acid and serum homocysteine increased obviously, genetic analysis revealed a heterozygous MMACHC mutation (exonl: c. 80A >G, c. 609G >A). The final diagnosis was aHUS induced by inherited methylmalonic acidemia (MMACHC heterozygous mutation exonl: c. 80A >G, c. 609G >A).Interventions:The patient was treated with a 1mg vitamin B12 intramuscular injection daily for 4 days after which the dose was then adjusted to a 1mg intramuscular injection twice a week. At the same time, the girl was given levocarnitine, betaine, folic acid, along with supportive treatment.Outcomes:After treated by vitamin B12 for 10 days, the patient condition significantly improved, Follow-up results showed complete recovery of hemoglobin and renal function.Lessons:Although the majority of MMA onset from neurological damage, our case illustrates that partial CblC-type MMA can onset with severe metabolic aHUS. On the basis of chronic thrombotic microangiopathy (TMA)-induced renal damage, it can be complicated by acute hemolytic lesions. MMA should be considered in those patients with unclear microangiopathic hemolytic anemia accompany significant megaloblastic degeneration in bone marrow. We should pay attention to the causes and adopt a reasonable treatment strategy.

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Section: Discussionmentioning

confidence: 99%

Atypical hemolytic uremic syndrome induced by CblC subtype of methylmalonic academia

et al. 2017

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“…While few studies have directly linked the presence of a Clostridium infection to initiation of T1DM [104,105], a very large number of studies have implicated dysregulation in the number and types of gut Clostridia. In particular, Bifidobacteria, Bacteroides, and Lactobacilli all decrease significantly, while the number of Clostridia increases and is directly correlated with the degree of glucose dysregulation observed in the patient [26,37,[106][107][108][109][110][111].…”

Section: Relationship Of the Experimental Findings To Previous Resultsmentioning

confidence: 99%

Clostridia and Enteroviruses as Synergistic Triggers of Type 1 Diabetes Mellitus

Root-Bernstein,

Chiles,

Huber

et al. 2023

IJMS

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What triggers type 1 diabetes mellitus (T1DM)? One common assumption is that triggers are individual microbes that mimic autoantibody targets such as insulin (INS). However, most microbes highly associated with T1DM pathogenesis, such as coxsackieviruses (COX), lack INS mimicry and have failed to induce T1DM in animal models. Using proteomic similarity search techniques, we found that COX actually mimicked the INS receptor (INSR). Clostridia were the best mimics of INS. Clostridia antibodies cross-reacted with INS in ELISA experiments, confirming mimicry. COX antibodies cross-reacted with INSR. Clostridia antibodies further bound to COX antibodies as idiotype–anti-idiotype pairs conserving INS–INSR complementarity. Ultraviolet spectrometry studies demonstrated that INS-like Clostridia peptides bound to INSR-like COX peptides. These complementary peptides were also recognized as antigens by T cell receptor sequences derived from T1DM patients. Finally, most sera from T1DM patients bound strongly to inactivated Clostridium sporogenes, while most sera from healthy individuals did not; T1DM sera also exhibited evidence of anti-idiotype antibodies against idiotypic INS, glutamic acid decarboxylase, and protein tyrosine phosphatase non-receptor (islet antigen-2) antibodies. These results suggest that T1DM is triggered by combined enterovirus-Clostridium (and possibly combined Epstein–Barr-virus-Streptococcal) infections, and the probable rate of such co-infections approximates the rate of new T1DM diagnoses.

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“…They discovered differences in microbial population dynamics in animals with kidney disease, such as increased alpha diversity, relative decreases in Lachnospiraceae and Lactobacillus , and increases in some Clostridia and opportunistic taxa. Although few studies have directly linked Clostridium infection to type 1 diabetes mellitus (T1DM) initiation [ 36 , 37 ], many studies have suggested that disturbance of Clostridia is related to glucose dysregulation in patients [ 38 - 44 ]. Our study is among the few to explore the abundance of Clostridia at the class level in DN.…”

Section: Discussionmentioning

confidence: 99%

Specific Alternation of Gut Microbiota and the Role of Ruminococcus gnavus in the Development of Diabetic Nephropathy

Hong,

Fu,

Liu

et al. 2023

J. Microbiol. Biotechnol.

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In this study, we aim to investigate the precise alterations in the gut microbiota during the onset and advancement of diabetic nephropathy (DN) and examine the impact of Ruminococcus gnavus ( R. gnavus ) on DN. Eight-week-old male KK-Ay mice were administered antibiotic cocktails for a duration of two weeks, followed by oral administration of R. gnavus for an additional eight weeks. Our study revealed significant changes in the gut microbiota during both the initiation and progression of DN. Specifically, we observed a notable increase in the abundance of Clostridia at the class level, higher levels of Lachnospirales and Oscillospirales at the order level, and a marked decrease in Clostridia_UCG-014 in DN group. Additionally, there was a significant increase in the abundance of Lachnospiraceae, Oscillospiraceae, and Ruminococcaceae at the family level. Moreover, oral administration of R. gnavus effectively aggravated kidney pathology in DN mice, accompanied by elevated levels of urea nitrogen (UN), creatinine (Cr), and urine protein. Furthermore, R. gnavus administration resulted in down-regulation of tight junction proteins such as Claudin-1, Occludin, and ZO-1, as well as increased levels of uremic toxins in urine and serum samples. Additionally, our study demonstrated that orally administered R. gnavus up-regulated the expression of inflammatory factors, including nucleotide-binding oligomerization domain-like receptor pyrin domain-containing protein 3 (NLRP3) and Interleukin (IL)-6. These changes indicated the involvement of the gut-kidney axis in DN, and R. gnavus may worsen diabetic nephropathy by affecting uremic toxin levels and promoting inflammation in DN.

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Hemolytic uremic syndrome complicated by Clostridium septicum bacteremia and new-onset type 1 diabetes mellitus. Report of a case

Cited by 5 publications

References 0 publications

Atypical hemolytic uremic syndrome induced by CblC subtype of methylmalonic academia

Atypical hemolytic uremic syndrome induced by CblC subtype of methylmalonic academia

Clostridia and Enteroviruses as Synergistic Triggers of Type 1 Diabetes Mellitus

Specific Alternation of Gut Microbiota and the Role of Ruminococcus gnavus in the Development of Diabetic Nephropathy

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