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Central venous catheter infection-related glomerulonephritis under long-term parenteral nutrition: a report of two cases.

Okada M, Sato M, Ogura M, Kamei K, Matsuoka K, Ito S - BMC Res Notes (2016)

Bottom Line: One of them recovered completely following the removal of catheter and administration of antibiotics, while another did not respond to the treatments.She responded well, and achieved complete remission.If a patient is resistant to such conventional therapy, additional steroid and/or immunosuppressive agent could be considered.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology and Rheumatology, National Center for Child Health and Development, Tokyo, Japan. mapun_happy@yahoo.co.jp.

ABSTRACT

Background: Advances in long-term parenteral nutrition via indwelling central venous catheter have improved the quality of life and mortality in patients with life-threatening gastrointestinal diseases complicated with severely impaired absorption. However, infection to central venous catheter is still a common and critical complication for such patients. We encountered two patients under long-term parenteral nutrition who developed glomerulonephritis associated with central venous catheter infection. Persistent bacterial infection in indwelling medical devices placed in the blood-stream such as a ventricular-atrial shunt is known to cause glomerulonephritis, a condition termed shunt nephritis. We reported the clinical manifestations, treatment and their pathological findings in the two patients with glomerulonephritis associated with central venous catheter infection.

Case presentation: Both patients suffered from megacystis microcolon intestinal hypoperistalsis syndrome, a form of pseudo-Hirschsprung's disease. They had been receiving home parenteral nutrition via central venous catheter because of severe malabsorption. They presented proteinuria, hematuria, hypocomplementemia and positive PR3-antineutrophilic cytoplasmic antibody accompanied by Staphylococcus epidermidis infection in the central venous catheter. Their renal biopsy revealed membranoproliferative glomerulonephritis with positive C3 deposition. One of them recovered completely following the removal of catheter and administration of antibiotics, while another did not respond to the treatments. We then treated her with methylprednisolone pulse therapy followed by prednisolone. She responded well, and achieved complete remission.

Conclusion: As central venous catheter infection-related glomerulonephritis has a similar etiology to shunt nephritis, removal of the catheter and administration of antibiotics is fundamental to the treatment. If a patient is resistant to such conventional therapy, additional steroid and/or immunosuppressive agent could be considered. Although the number of patients with classical shunt nephritis is decreasing since the ventricular-peritoneal shunt has become became the major procedure for hydrocephalus, central venous catheter infection-related glomerulonephritis may increase in the future due to a marked increase in the number of patients receiving long-term parenteral nutrition. Routine urinalysis should be considered in such patients for early detection of central venous catheter infection-related glomerulonephritis.

No MeSH data available.


Related in: MedlinePlus

First biopsy of patient 2: a (PAS stain, magnification ×400); b (PAM stain, magnification ×400), mesangial proliferation, increased lobulation, doubled contours: c (electron microscopy), subepithelial, subendothelial, mesangial deposit: d (immuno-fluorescence microscopy), C3 (++), IgM (++), C1q (+), IgG (+) fringe pattern
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Fig1: First biopsy of patient 2: a (PAS stain, magnification ×400); b (PAM stain, magnification ×400), mesangial proliferation, increased lobulation, doubled contours: c (electron microscopy), subepithelial, subendothelial, mesangial deposit: d (immuno-fluorescence microscopy), C3 (++), IgM (++), C1q (+), IgG (+) fringe pattern

Mentions: On admission, her height was 159.4 cm, and body weight was 45.8 kg. Her blood pressure was 110/82 mmHg, and her chest and abdomen exhibited no abnormal findings. Blood examination revealed hypoalbuminemia (serum albumin, 2.5 g/dL), renal insufficiency (serum creatinine, 0.92 mg/dL, Cys-C 1.69 mg/L, e-GFR, 63.1 mL/min/1.73 m2, hypocomplementemia (C3, 57 mg/dL; C4, 24 mg/dL; and CH50, 10.5 U/mL) and positive PR3-ANCA (19 U/mL; normal range 0-9 U/mL). Urinalysis revealed proteinuria (urinary protein 29.1 mg/dL, urinary creatinine 18.7 mg/dL), and hematuria (30–49 erythrocytes per high power field). Blood cultures did not reveal S. epidermidis (MRSE) colonization in the peripheral blood but in the CVC instead. After admission, we immediately removed the CVC and started antibiotics for 7 days. Her fever was soon resolved, but proteinuria, hematuria and renal insufficiency continued. Renal biopsy was performed 18 days after admission (Fig. 1). LM revealed diffuse mesangial proliferation, lobulation in the glomeruli, endocapillary proliferation and double contours in the glomerular capillary. Two of 18 glomeruli showed global glomerular sclerosis. Immunofluorescence microscopy revealed deposits of C3 and IgM with fringe pattern along the glomerular capillary. EM revealed subepithelial, subendothelial, and intra-basement membrane electron-dense deposits. These biopsy findings are compatible with membranoproliferative glomerulonephritis. After several blood cultures that proved to be negative, she was treated with two courses of methylprednisolone pulse therapy followed by 40 mg prednisolone daily for 1 month. Afterwards, prednisolone was reduced to 40 mg every other day and gradually decreased over 8 months. She responded well to these treatments, urinary findings and renal function completely recovered in 9 months (Fig. 2b). She remains free from medication without further recurrence of proteinuria and hematuria.Fig. 1


Central venous catheter infection-related glomerulonephritis under long-term parenteral nutrition: a report of two cases.

Okada M, Sato M, Ogura M, Kamei K, Matsuoka K, Ito S - BMC Res Notes (2016)

First biopsy of patient 2: a (PAS stain, magnification ×400); b (PAM stain, magnification ×400), mesangial proliferation, increased lobulation, doubled contours: c (electron microscopy), subepithelial, subendothelial, mesangial deposit: d (immuno-fluorescence microscopy), C3 (++), IgM (++), C1q (+), IgG (+) fringe pattern
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4815057&req=5

Fig1: First biopsy of patient 2: a (PAS stain, magnification ×400); b (PAM stain, magnification ×400), mesangial proliferation, increased lobulation, doubled contours: c (electron microscopy), subepithelial, subendothelial, mesangial deposit: d (immuno-fluorescence microscopy), C3 (++), IgM (++), C1q (+), IgG (+) fringe pattern
Mentions: On admission, her height was 159.4 cm, and body weight was 45.8 kg. Her blood pressure was 110/82 mmHg, and her chest and abdomen exhibited no abnormal findings. Blood examination revealed hypoalbuminemia (serum albumin, 2.5 g/dL), renal insufficiency (serum creatinine, 0.92 mg/dL, Cys-C 1.69 mg/L, e-GFR, 63.1 mL/min/1.73 m2, hypocomplementemia (C3, 57 mg/dL; C4, 24 mg/dL; and CH50, 10.5 U/mL) and positive PR3-ANCA (19 U/mL; normal range 0-9 U/mL). Urinalysis revealed proteinuria (urinary protein 29.1 mg/dL, urinary creatinine 18.7 mg/dL), and hematuria (30–49 erythrocytes per high power field). Blood cultures did not reveal S. epidermidis (MRSE) colonization in the peripheral blood but in the CVC instead. After admission, we immediately removed the CVC and started antibiotics for 7 days. Her fever was soon resolved, but proteinuria, hematuria and renal insufficiency continued. Renal biopsy was performed 18 days after admission (Fig. 1). LM revealed diffuse mesangial proliferation, lobulation in the glomeruli, endocapillary proliferation and double contours in the glomerular capillary. Two of 18 glomeruli showed global glomerular sclerosis. Immunofluorescence microscopy revealed deposits of C3 and IgM with fringe pattern along the glomerular capillary. EM revealed subepithelial, subendothelial, and intra-basement membrane electron-dense deposits. These biopsy findings are compatible with membranoproliferative glomerulonephritis. After several blood cultures that proved to be negative, she was treated with two courses of methylprednisolone pulse therapy followed by 40 mg prednisolone daily for 1 month. Afterwards, prednisolone was reduced to 40 mg every other day and gradually decreased over 8 months. She responded well to these treatments, urinary findings and renal function completely recovered in 9 months (Fig. 2b). She remains free from medication without further recurrence of proteinuria and hematuria.Fig. 1

Bottom Line: One of them recovered completely following the removal of catheter and administration of antibiotics, while another did not respond to the treatments.She responded well, and achieved complete remission.If a patient is resistant to such conventional therapy, additional steroid and/or immunosuppressive agent could be considered.

View Article: PubMed Central - PubMed

Affiliation: Division of Nephrology and Rheumatology, National Center for Child Health and Development, Tokyo, Japan. mapun_happy@yahoo.co.jp.

ABSTRACT

Background: Advances in long-term parenteral nutrition via indwelling central venous catheter have improved the quality of life and mortality in patients with life-threatening gastrointestinal diseases complicated with severely impaired absorption. However, infection to central venous catheter is still a common and critical complication for such patients. We encountered two patients under long-term parenteral nutrition who developed glomerulonephritis associated with central venous catheter infection. Persistent bacterial infection in indwelling medical devices placed in the blood-stream such as a ventricular-atrial shunt is known to cause glomerulonephritis, a condition termed shunt nephritis. We reported the clinical manifestations, treatment and their pathological findings in the two patients with glomerulonephritis associated with central venous catheter infection.

Case presentation: Both patients suffered from megacystis microcolon intestinal hypoperistalsis syndrome, a form of pseudo-Hirschsprung's disease. They had been receiving home parenteral nutrition via central venous catheter because of severe malabsorption. They presented proteinuria, hematuria, hypocomplementemia and positive PR3-antineutrophilic cytoplasmic antibody accompanied by Staphylococcus epidermidis infection in the central venous catheter. Their renal biopsy revealed membranoproliferative glomerulonephritis with positive C3 deposition. One of them recovered completely following the removal of catheter and administration of antibiotics, while another did not respond to the treatments. We then treated her with methylprednisolone pulse therapy followed by prednisolone. She responded well, and achieved complete remission.

Conclusion: As central venous catheter infection-related glomerulonephritis has a similar etiology to shunt nephritis, removal of the catheter and administration of antibiotics is fundamental to the treatment. If a patient is resistant to such conventional therapy, additional steroid and/or immunosuppressive agent could be considered. Although the number of patients with classical shunt nephritis is decreasing since the ventricular-peritoneal shunt has become became the major procedure for hydrocephalus, central venous catheter infection-related glomerulonephritis may increase in the future due to a marked increase in the number of patients receiving long-term parenteral nutrition. Routine urinalysis should be considered in such patients for early detection of central venous catheter infection-related glomerulonephritis.

No MeSH data available.


Related in: MedlinePlus