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\begin{document}

             \author[1]{Awad Magbri,  MD}

             \affil[1]{  PINE (partners in Nephrology and Endocrinology}

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\date{\small \em Received: 8 December 2015 Accepted: 1 January 2016 Published: 15 January 2016}

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\begin{abstract}
        


Case-The case is that of 52 year Caucasian male with motor vehicle accident, status post open reduction and internal fixation of the left hip. He sustained wound infection with osteomyelitis due to multidrug resistant pseudomonas infection. Extensive debridement of the wound was carried out but the hardware was left in place. He underwent treatment with polymyxin antibiotic for a month then the course was complicated by renal failure which resolved with polymyxin dose adjustment. However, the hard ware was removed after 2 months of treatment. At that time wound culture revealed MRSA infection.He received 4 weeks of Vancomycin and 6 week course of polymyxin after the hardware was removal. He was readmitted to the hospital with increasing pain and persistent drainage from the wound. Imagings were consistent with erosion of the femoral head with joint space loss, and septic arthritis with evidence of osteomyelitis and the presence of sinus tract to the skin surface. Wash out of the wound with debridement was carried out and another course of Vancomycin was instituted.

\end{abstract}


\keywords{staphylococcal associated glomerulonephritis, IgA nephropathy, hypocomplementemia, MRSA, endocapillary proliferation, mesangial staining.}

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\let\tabcellsep& 	 	 		 
\section[{I. Case}]{I. Case}\par
he case is that of 52 year Caucasian male with motor vehicle accident, status post open reduction and internal fixation of the left hip. He sustained wound infection with osteomyelitis due to multidrug resistant pseudomonas infection. Extensive debridement of the wound was carried out but the hardware was left in place. He underwent treatment with polymyxin antibiotic for a month then the course was complicated by renal failure which resolved with polymyxin dose adjustment. However, the hard ware was removed after 2 months of treatment. At that time wound culture revealed MRSA infection.\par
He received 4 weeks of Vancomycin and 6 week course of polymyxin after the hardware was removal. He was readmitted to the hospital with increasing pain and persistent drainage from the wound. Imagings were consistent with erosion of the femoral head with joint space loss, and septic arthritis with evidence of osteomyelitis and the presence of sinus tract to the skin surface. Wash out of the wound with debridement was carried out and another course of Vancomycin was instituted.\par
He developed worsening renal function with increasing creatinine from 1.2 to 6.7 mg/dl over 4 week period. His past medical history was positive for type II diabetes, hypertension, anemia, and hyperlipedemia. His medication consisted of insulin, lisinopril, iron, folic acid, omeprazole, and subcutaneous heparin. His review of system was positive for dark urine and leg swelling.\par
He was hypertensive on physical examination with BP 150/89 mmHg; afebrile and other wise examination of the cardiovascular, respiratory and abdomen were unremarkable. He had mild swelling of the left hip with surgical scar with chronic skin changes but no drainage. The examination also showed 3+ edema of the lower extremities.\par
His laboratory results showed WBC 11.4 with 73\% PMN, Hg 7.8, and platelets of 332K. He had low albumin of 2.4 g/dl and phosphorus of 6.0 mg/dl. The serum creatinine had risen from 1.2 to 8.9 in 2 month's time. Urine protein was 2 gm/day and his UA showed protein >300 mg/dl, WBC 2-5, RBC packed, fine granular casts and RBC casts. His serology was negative for HIV, Hepatitis B and C, ANA, dsDNA, RF, ANCA.\par
His kidney biopsy revealed nodular mesangial sclerosis with necrotizing crescentic glomerulonephritis. The immunofluorescent (IF) staining of the kidney tissue showed 3+ IgA, 3+ C3. His complements C3, C4 were within normal limits and his urine immunofixation was negative.\par
Electron microscopy (EM) of renal specimen revealed deposition of immune-dense materials in the mesangium and in the subepithelia spaces. The final diagnosis was MRSA associated post-infectious glomerulonephritis.\par
Differential diagnoses: IgA nephropathy, post-infectious glomerulonephritis, pausi-immune ANCA associated nephritis, and MRSA post-infectious glomerulonephritis. 
\section[{II. Discussion}]{II. Discussion}\par
There  \hyperref[b1]{(2)}. The antigenantibody complexes deposit in the mesangium and subepithelium forming humps on electron microscopical examination. There are few reports on MRSA induced glomerulonephritis in the literature \hyperref[b6]{(7)}\hyperref[b7]{(8)}\hyperref[b8]{(9)}. Acute infectious glomerulonephritis is different when presented in adult patients.\par
The mean age of presentation is 49-58 years, and commonly associated with underlying co-morbidities in 40-50\% of patients \hyperref[b9]{(10)}. These comorbidities include alcoholism in 2-57\%, diabetes in 8-29\%, COPD in 7-33\%, IV drug use in 3-27\%, and malignancy in 5-10\% (13) Table-1.\par
SAGN associated glomerulonephritis has protean manifestation including nephritic syndrome in 60\%, nephrotic syndrome with gross proteinuria in 30-50\%, the mean serum 24 hrs protein is 3.6 g/24 hrs which increases with increasing co-morbidities, and the mean serum creatinine in one series is 1.6-6.4 mg/dl, Table-1. The laboratory findings at the time of presentation are similar to those findings in other forms of glomerulonephritis \hyperref[b7]{(8)}. Hematuria in 98\%, leukocytoria in 65\%, mean protein excretion -3 g/day (21\% had all features of nephrotic syndrome), and the mean serum creatinine at the time of biopsy -5.1 mg/dl. Table \hyperref[tab_2]{-1} Kidney biopsy in these cases show Endocapillary proliferation in 70-100\% of cases, crescents more than (20-30\%) of the glomeruli in 14-36\%, interstitial infiltration in 30-80\%, and evidence of ATN in 20-40\%.\par
Immunofluorescent staining showed granular staining and deposition of IgG and C3 or C3 alone in a peripheral capillary wall and mesangial distribution. IgA usually is absent or has less trace positivity on peripheral capillary walls \hyperref[b10]{(11)}. IF deposits are C3 in 93-100\%, C1q in 18-35\%, IgG in 55-65\%, and IgM/IgA in 30-45\% of cases, \hyperref[b10]{(11)}\hyperref[b11]{(12)}\hyperref[b12]{(13)}\hyperref[b13]{(14)}\hyperref[b14]{(15)}\hyperref[b15]{(16)}\hyperref[b16]{(17)}\hyperref[b17]{(18)}, Table-1.\par
The IF findings in this disease resemble those typically seen in patients with IgA nephropathy or Henoch-Schonlein purpura nephritis, however, the presence of hypocomplementemia, concurrent culture positive bacterial infection, and light microscopic pattern of diffuse Endocapillary hypercellularity with marked neutrophil infiltration in addition to mesangial and subendothelial deposits strongly favor acute post-infectious glomerulonephritis over IgA nephropathy, Table \hyperref[tab_2]{-2}.\par
The EM study reveals mesangial deposits in 33-90\%, sub-endothelial deposits in 44-75\%, and sunendothelial humps in 94-100\% of cases \hyperref[b10]{(11)}.\par
The major diagnostic criteria should include at least 2 of the followings (11-13);\par
? Hypocomplementemia (primary low C3)  
\section[{III. Course of Disease and Prognosis}]{III. Course of Disease and Prognosis}\par
Successful eradication of the infection should result in resolution of GN. However, many patients with SAGN do not have complete resolution of the serum creatinine to baseline and will have persistent proteinuria. In one series (9) 50\% of patients attained complete resolution of the disease. Older age and presence of co-morbid conditions like DM with high serum creatinine at presentation portend worse prognosis \hyperref[b7]{(8,}\hyperref[b8]{9)}.\par
In a study of 86 adults followed for 48 months in 41 patients without DM, 23/42(56\%) attain complete remission, 11/41(27\%) had persistent renal dysfunction, and 7/41(17\%) progressed to ESRD requiring renal replacement therapy. The renal prognosis is worse in patients with DM among 11 patients with SAGN2/11 had persistent renal dysfunction and 9/11 progressed to ESRD \hyperref[b14]{(15,} {\ref 23,} {\ref 24)}.\par
In another report in elderly patients with SAGN (mean age 65 years) 34/109 were followed up for at least 3 months (11), 24\% had complete recovery of renal function, 32\% had persistent renal dysfunction, and 44\% progressed to ESRD. Tubular atrophy and interstitial fibrosis are markers of chronic renal disease \hyperref[b10]{(11)}. \begin{figure}[htbp]
\noindent\textbf{-} \par 
\begin{longtable}{P{0.05400987045033929\textwidth}P{0.5196483652066625\textwidth}P{0.054534238124614436\textwidth}P{0.22180752621838373\textwidth}}
\tabcellsep \multicolumn{3}{l}{Staphylococcus Associated Glomerulonephritis with IgA Mesangial Deposition}\\
\tabcellsep Presentation ? Nephritic syndrome ? Nephrotic syndrome ? Mean serum creatinine ? Mean 24 hr protein\tabcellsep \multicolumn{2}{l}{60\% 30-50\% 1.5-6.4 mg/dl (increased with co-morbidities/crescentic GN) 3.6 g/24 hrs (increase with co-}\\
\tabcellsep Kidney biopsy\tabcellsep \tabcellsep morbidities)\\
\tabcellsep ? Endocapillary proliferation\tabcellsep \\
\tabcellsep ? Crescents (>20-30\%) ? Interstitial infiltration ? ATN IF staining:\tabcellsep \tabcellsep 70-100\% 14-36\% 30-80\% 20-40\%\\
Year 2016 Year 2016\tabcellsep ? C3 deposits ? C1q ? IgG deposits\tabcellsep \tabcellsep 93-100\% 18-35\%\\
\tabcellsep ? IgM/IgA\tabcellsep \tabcellsep 55-65\%\\
\tabcellsep EM\tabcellsep \tabcellsep 30-45\%\\
Volume XVI Issue V Version I Volume XVI Issue V Version I\tabcellsep ? Mesangial deposits ? Sub-endothelial ? Humps Sites of infection and microbiology ? URI ? SSTI ? Lungs ? Endocarditis ? Dental ? UTI Organisms\tabcellsep \tabcellsep 33-90\% 44-75\% 94-100\% 24-44\% 5-25\% 16-18\% 1-13\% 0-13\% 1-12\%\\
( D D D D ) F ( D D D D ) F\tabcellsep ? Streptococcus ? Staphylococcus\tabcellsep \tabcellsep 14-47\% 12-24\%\\
\tabcellsep ? Gram negative\tabcellsep \tabcellsep 1-22\%\\
\tabcellsep ? No growth\tabcellsep \tabcellsep 24-59\%\\
\tabcellsep \multicolumn{3}{l}{Table-2: differential from IgA nephropathy}\\
\tabcellsep Staphylococcal associated glomerulonephritis\tabcellsep \tabcellsep IgA nephropathy\\
\tabcellsep Older age at presentation with underlying DM\tabcellsep \tabcellsep Younger age group with hematuria\\
\tabcellsep Acute kidney injury at presentation\tabcellsep \tabcellsep Can occurs when there is gross hematuria\\
\tabcellsep Hypocomplementemia (mainly decrease C3)\tabcellsep \tabcellsep Not typically seen\\
\tabcellsep Diffuse exudative glomerulonephritis on LM\tabcellsep \tabcellsep Mesangial proliferative disease\\
\tabcellsep \multicolumn{2}{l}{Stronger intensity of IF staining for C3 than IgA in glomerular deposits}\tabcellsep Predominant global mesangial IgA staining\\
\tabcellsep Sub-epithelial humps on EM\tabcellsep \tabcellsep Mesangial deposits of IgA\\
\tabcellsep Characteristic\tabcellsep \tabcellsep Percentage\\
\tabcellsep Median age\tabcellsep \tabcellsep 49-50 years\\
\tabcellsep Underlying disease\tabcellsep \\
\tabcellsep ? Alcoholism +/\textunderscore  cirrhosis\tabcellsep \tabcellsep 2-57\%\\
\tabcellsep ? Diabetes\tabcellsep \tabcellsep 8-29\%\\
\tabcellsep ? COPD\tabcellsep \tabcellsep 7-33\%\\
\tabcellsep ? IVDU\tabcellsep \tabcellsep 3-27\%\\
\tabcellsep ? Malignancy\tabcellsep \tabcellsep 5-10\%\end{longtable} \par
 
\caption{\label{tab_2}Table - 1}\end{figure}
 			\footnote{© 2016 Global Journals Inc. (US)} 		 		\backmatter  			  				\begin{bibitemlist}{1}
\bibitem[Yoh et al. ()]{b3}\label{b3} 	 		‘A case of superantigen-related glomerulonephritis after methicillin-resistant Staphylococcus aureus (MRSA) infection’.  		 			K Yoh 		,  		 			M Kobayachi 		,  		 			A Hirayama 		.  	 	 		\textit{Clin Nephrol}  		1997. 48 p. .  	 
\bibitem[Nasr et al. ()]{b11}\label{b11} 	 		‘Acute post-infectious glomerulonephritis in modern era: experience with 86 adults and review of the literature’.  		 			S H Nasr 		,  		 			G S Markowitz 		,  		 			M B Stokes 		.  	 	 		\textit{Medicine (Baltimore)}  		2008. 87 p. 21.  	 
\bibitem[Nasr et al. ()]{b12}\label{b12} 	 		‘Bacterial infection-related glomerulonephritis in adults’.  		 			S H Nasr 		,  		 			J Radhakrishnan 		,  		 			D'agati Vd 		.  	 	 		\textit{Kidney Int}  		2013. 83 p. 792.  	 
\bibitem[Nagaba et al. ()]{b2}\label{b2} 	 		‘Effective antibiotic treatment of methicillin-resistant Staphylococcus aureus-associated glomerulonephritis’.  		 			Y Nagaba 		,  		 			Y Hiki 		,  		 			T Aoyama 		.  	 	 		\textit{Nephron}  		2002. 92 p. .  	 
\bibitem[Chirinos et al.]{b19}\label{b19} 	 		\textit{Endocarditis associated with antineutrophil},  		 			J A Chirinos 		,  		 			V F Corrales-Medina 		,  		 			S Garcia 		.  		 	 
\bibitem[Sorger et al. ()]{b15}\label{b15} 	 		‘Follow-up studies of three subtypes of acute postinfectious glomerulonephritis ascertained by renal biopsy’.  		 			K Sorger 		,  		 			M Gessler 		,  		 			F K Hubner 		.  	 	 		\textit{Clin Nephrol}  		1987. 27 p. 111.  	 
\bibitem[Spector et al. ()]{b6}\label{b6} 	 		‘Glomerulonephritis and Staphylococcal aureus infections’.  		 			D A Spector 		,  		 			J Millan 		,  		 			N Zauber 		,  		 			J Burton 		.  	 	 		\textit{Clin Nephrol}  		1980. 14 p. .  	 
\bibitem[Koyama et al. ()]{b1}\label{b1} 	 		‘Glomerulonephritis associated with MRSA infection: A possible role of bacterial superantigen’.  		 			A Koyama 		,  		 			M Kobayashi 		,  		 			N Yamaguchi 		.  	 	 		\textit{Kidney Int}  		1995. 47 p. .  	 
\bibitem[Handa et al. ()]{b7}\label{b7} 	 		‘Glomerulonephritis induced by methicillin-sensitive Staphylococcus aureus infection’.  		 			T Handa 		,  		 			T Ono 		,  		 			H Watanabe 		.  	 	 		\textit{Clin Exp Nephrol}  		2003. 7 p. .  	 
\bibitem[Nasr and Vd ()]{b16}\label{b16} 	 		‘IgA-dominant postinfectious glomerulonephritis: a new twist on an old disease’.  		 			S H Nasr 		,  		 			D'agati Vd 		.  	 	 		\textit{Nephron Clin Pract}  		2011. 119 p. 18.  	 
\bibitem[Nasr et al. ()]{b8}\label{b8} 	 		‘IgAdominant acute post-staphylococcal glomerulonephritis complicating diabetic nephropathy’.  		 			S H Nasr 		,  		 			G S Markowitz 		,  		 			J D Whelan 		.  	 	 		\textit{Hum Pathol}  		2003. 34 p. .  	 
\bibitem[Worawichawong et al. ()]{b17}\label{b17} 	 		‘immunoglobulin A-dominant postinfectious glomerulonephritis: frequent occurrence in nondiabetic patients with Staphylococcus aureus infection’.  		 			S Worawichawong 		,  		 			L Girard 		,  		 			K Trpkov 		.  	 	 		\textit{Hum pathol}  		2011. 42 p. 279.  	 
\bibitem[Maroni et al. ()]{b9}\label{b9} 	 		‘Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults’.  		 			G Maroni 		,  		 			C Pozzi 		,  		 			S Guaglini 		.  	 	 		\textit{Nephrol Dial Transplant}  		2002. 17 p. 1204.  	 
\bibitem[Nasr et al. ()]{b10}\label{b10} 	 		‘Postinfectious glomerulonephritis in the elderly’.  		 			S H Nasr 		,  		 			M E Fidler 		,  		 			A M Valeri 		.  	 	 		\textit{J Am Soc Nephrol}  		2011. 22 p. 187.  	 
\bibitem[Samtleben et al. ()]{b0}\label{b0} 	 		‘Renal complications of infected shunts’.  		 			W Samtleben 		,  		 			G Bauriedal 		,  		 			T Bosch 		.  	 	 		\textit{Artif Organs}  		1993. 17 p. .  	 
\bibitem[Staphylococcus Associated Glomerulonephritis with IgA Mesangial Deposition endocarditis in heroin addict Am J Nephrol ()]{b5}\label{b5} 	 		‘Staphylococcus Associated Glomerulonephritis with IgA Mesangial Deposition endocarditis in heroin addict’.  	 	 		\textit{Am J Nephrol}  		1987. 7 p. .  	 
\bibitem[Satoskar et al. ()]{b14}\label{b14} 	 		‘Staphylococcus infection-associated glomerulonephritis mimicking IgA nephropathy’.  		 			A A Satoskar 		,  		 			G Nadasdy 		,  		 			J A Plaza 		.  	 	 		\textit{Clin J Am Soc Nephrol}  		2006. 1 p. 1179.  	 
\bibitem[Choi et al. ()]{b18}\label{b18} 	 		‘Subacute bacterial endocarditis with positive cytoplasmic antineutrophil cytoplasmic antibodies and antiproteinase 3 antibodies’.  		 			H K Choi 		,  		 			P Lamprecht 		,  		 			J L Niles 		.  	 	 		\textit{Arthritis Rheum}  		2000. 43 p. 226.  	 
\bibitem[Sato et al. ()]{b4}\label{b4} 	 		‘The pathogenetic role of Staphylococcus aureus in primary human glomerulonephritis’.  		 			M Sato 		,  		 			H Nakazora 		,  		 			T Ofuji 		.  	 	 		\textit{Clin Nephrol}  		1979. 11 p. .  	 
\bibitem[Wen and Chen ()]{b13}\label{b13} 	 		‘The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis’.  		 			Y K Wen 		,  		 			M L Chen 		.  	 	 		\textit{Clin Nephrol}  		2010. 73 p. 173.  	 
\end{bibitemlist}
 			 		 	 
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