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A rare clinical case of penile gangrene in a patient with chronic renal failure and diabetes mellitus.

ABSTRACT: We report here a case of penile gangrene due to penile calciphylaxis in a patient with diabetes mellitus and chronic renal failure. Initially the patient demonstrated dry gangrene of the glans penis, which turned to wet after partial amputation. The main cause of the gangrene was considered to be circulatory insufficiency induced by severe arteriosclerosis. Despite high mortality rate associated with ischaemic penile gangrene aggressive management is recommended for those who are not terminal.

SUBMITTER: Dunev VR

PROVIDER: S-EPMC6370555 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature

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A rare clinical case of penile gangrene in a patient with chronic renal failure and diabetes mellitus.

Dunev V R VR Kolev N H NH Genov P P PP

Urology case reports 20190131

We report here a case of penile gangrene due to penile calciphylaxis in a patient with diabetes mellitus and chronic renal failure. Initially the patient demonstrated dry gangrene of the glans penis, which turned to wet after partial amputation. The main cause of the gangrene was considered to be circulatory insufficiency induced by severe arteriosclerosis. Despite high mortality rate associated with ischaemic penile gangrene aggressive management is recommended for those who are not terminal. ...[more]

PMID: 30805296

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Project description:BackgroundPost-transplant diabetes mellitus (PTDM) is an emerging problem in kidney transplantation, representing an important risk factor for kidney function loss. Diabetic nephropathy (DN) occurrence in transplanted kidneys is poorly investigated. Current knowledge describes DN recurrence in graft 5.9 years from kidney transplantation however there is little data about PTDM and DN. Here, we report a clinical case peculiar for an early appearance of advanced glomerular diabetic lesions, after kidney transplantation.Case presentationA 45-year-old Caucasian male affected by autosomal polycystic kidney disease was transplanted with a cadaveric-kidney-donor from 58-year-old male. Induction immunosuppressive therapy included basiliximab and steroids while the maintenance treatment included, tacrolimus, mofetil micophenolate and methylprednisolone. One month after transplantation the patient developed diabetes requiring treatment with repaglinide quickly replaced with insulin to obtain an acceptable glycemic control (HbA1c 52 mmol/mol). Glycosuria was detected persistently during the first six months after transplantation. To achieve further improvement in glycemic control, a shift from tacrolimus to cyclosporine (CyA) was made and steroids were rapidly tapered and stopped. To minimize calcineurin inhibitors toxicity, which was revealed in the 1-year-protocol-biopsy, everolimus was introduced thereby lowering CyA through levels. Moderate hypertension was well controlled with doxazosin. Thirty months after transplantation a second graft biopsy was performed owing to renal function decline and microalbuminuria appearance. Histological analysis surprisingly showed mesangiolysis and microaneurysms; glomerular sclero-hyalinosis and basal membrane thickness and typical nodular glomerulosclerosis. C4d staining was negative and no evidence of immune deposits were detected. Donor Specific Antibodies, serum C3 and C4 levels and autoimmunity tests were negative. Retrospective analysis on donor history didn't show diabetes or insulin resistance and no diabetic lesions were found in kidney pre-implant biopsy.ConclusionsIn our knowledge, this is the first report describing a very early onset of advanced diabetic glomerular lesions in a graft biopsy after PTDM. We hypothesize that additional factors such as everolimus and hypertension, may have contribute to kidney damage.

Project description:Objective: This study aimed to investigate the clinical and molecular biology of a patient with a type of diabetes mellitus caused by a mutation in the POC1A (OMIM number: 614783) gene and explore its pathogenesis and related characteristics. Methods: The patient was interviewed about his medical history and subjected to relevant examinations. Blood DNA samples were collected from the patient and his family members (parents) for trio whole-exome sequencing. Whole-exome sequencing was performed using the IDT xGen Exome Research Panel v1.0 whole-exome capture chip and sequenced using an Illumina NovaSeq 6,000 series sequencer (PE150); the sequencing coverage of the target sequence was not less than 99%. After systematic analysis and screening of the cloud platform for accurate diagnosis of genetic diseases, which integrated molecular biology annotation, biology, genetics, and clinical feature analysis, combined with a pathogenic mutation database, normal human genome database, and clinical feature database of 4,000 known genetic diseases, hundreds of thousands of gene variants were graded using the gene data analysis algorithm, a three-element grading system, and the American Society of Medical Genetics gene variant grading system. After polymerase chain reaction testing, the target sequence was verified by Sanger sequencing using an ABI3730 sequencer, and the verification result was obtained using sequence analysis software. Results: The patient had a peculiar face, a thin body, and a body mass index of 16.0 kg/m2. His fasting connecting peptide was 10.2 ug/L, his fasting insulin was 44 mIU/L, his fasting blood glucose was 10.5 mmol/L, and his glycosylated haemoglobin was 12.5%. After hospitalisation, the patient was given 0.75 g/d metformin tablets and 15 mg/d pioglitazone dispersible tablets, and his fasting blood glucose reduced to 9.2 mmol/L. After 48 U/L insulin treatment, the patient's fasting blood glucose was reduced to 8.5 mmol/L. Genetic screening revealed that there was a pathogenic variant at the POC1A gene locus and a cytosine-to-thymine mutation at the G81 locus, turning the Arg to a termination codon and shortening the POC1A protein from 359 amino acids (aa) to 80 aa. No mutation was detected in the patient's parents' POC1A gene loci. Conclusion: The patient's diabetes was caused by a POC1A gene mutation at the G81 locus, which is rarely reported in the clinic. The specific manifestations of this mutation need to be further investigated.

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A rare clinical case of penile gangrene in a patient with chronic renal failure and diabetes mellitus.

Publications

A rare clinical case of penile gangrene in a patient with chronic renal failure and diabetes mellitus.

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