Cellulitis with IgA Glomerulonephritis
The patient was started on vancomycin in the emergency room, which was later renally dosed during his hospitalization. His creatinine reached a peak of 3.7 (GFR 21) and he remained in the hospital for six days. He was discharged with an outpatient regimen of levofloxacin and minocycline. His creatinine returned to near baseline (1.59), three weeks after discharge.
During his admission, he gained twenty pounds of fluid. He likely had a nephrotic component to his renal injury, however no urine protein levels were obtained during his hospital stay. A random urinalysis sample was obtained from his nephrologist at his one week hospital follow-up visit that revealed 750mg of protein in his urine.
Following discharge, A.C. began to aggressively train for his senior year football season, working out fifteen to twenty hours each week with the college ATCs. One week after discharge, he developed atypical sub-sternal chest pain. The pain was initially intermittent, and he believed it was related to training. When the pain became constant, approximately six weeks after discharge, the patient alerted his athletic trainers who brought him into the training room. He was referred to cardiology who diagnosed AC with pericarditis just two weeks before the start of summer football training.
Now with Stage III, CKD (Cr 1.6 - 1.8, GFR 50s) and pericarditis, his nephrologist recommended against playing football given his current state of health. For athletes with chronic kidney disease, return-to-play decisions are made based on each individual case. The previous football season had moved him into Stage II, CKD and during that season, he required the use of two anti-hypertensive agents and phosphorous binders. After developing cellulitis, fluid overload, and pericarditis, a long discussion was had between the athlete, his coaches, and his health care providers about his senior football season. The patient decided to retire from football for his health. He currently remains in Stage III, CKD and is interested in a career in Sports PT. He acted as an assistant coach on the football team for his senior year.
IgA nephropathy (Berger's disease) is the most common cause of primary glomerulonephritis. It has a peak incidence in the 2nd and 3rd decades of life, affecting males more than females (2:1). Mesangial deposits of IgA attract more IgA immune complexes leading to nephron damage, sclerosis and interstitial fibrosis that cause episodes of painless hematuria, often associated with infections or vigorous exercise. Diagnosis requires a renal biopsy. Nephrotic syndrome is rarely present and appears in only about 10% of cases.
The etiology of IgA Nephropathy is still unclear. Some theories propose a mutation in IgA genes, prior infections with a robust immune response, autoimmune disease due to dysregulation of IgA, and now even food allergies as possible causes of the disease. Prognosis is roughly divided into thirds, with one third going into remission, one third having progressive CKD over the course of their lives, and one third suffering complete renal failure. Renal failure often occurs over a 20-25 year course of progressively worsening CKD. Risk factors for loss of renal function include hypertension, presence of proteinuria (>1gm/day), older age at time of diagnosis, extensive fibrosis on renal biopsy, and being a male.
The decision for any athlete with CKD to return to play is made on an individual basis. To preserve renal function, a patient (or athlete) must maintain strict blood pressure control, reduce dietary protein intake, monitor potassium levels, and avoid nephrotoxic substances. Hypertension accelerates damage to the nephron. During high intensity training or games, an offensive lineman, like our case study A.C., can reach systolic blood pressures in excess of 180 - 200mmHg during tackles. Anti-hypertensive agents are utilized to control baseline blood pressure. During the playing season, additional agents or increasing daily dosing of existing agents may be necessary to maintain blood pressure control. Pre- and post-exertion blood pressure monitoring is recommended to ensure adequate control. A.C. required an additional antihypertensive agent during his junior year of football.
As the kidneys ability to excrete and filter substances declines, monitoring potassium and phosphorous, limiting protein intake and avoiding nephrotoxic substances becomes important for patients and athletes with CKD. Many anti-hypertensive agents can deplete potassium, while athletes may experience elevated potassium levels due to muscle breakdown. Decreased excretion occurs even in the presence of an antihypertensive agent, can lead to excess serum potassium. Likewise, phosphorous can also accumulate in the athlete. Phosphorous levels are kept low by imploring a low-protein (0.7gm/kg body mass). As phosphorous levels increase in the blood, it triggers secondary hyperparathyroidism and can ultimately disrupt the calcium/bone homeostasis. In addition to dietary intake, phosphorous binders can be used to help reduce phosphorous levels while maintaining normal PTH and calcium levels. Current trends are to avoid calcium-based phosphorous binders, as new research suggests increased intake of calcium may enhance coronary arterial calcification. Furthermore, avoidance of nephrotoxic substances such as NSAIDs and supplements as the kidneys have a decreased ability to excrete and filter these substances.
In summary, basic parameters for sports medicine physicians who care for athletes with CKD should ensure tight blood pressure control, monitor potassium and phosphorous, encourage a low-protein diet and teach patients to avoid nephrotoxic substances. Athletes and sports medicine practitioners may find the restriction of dietary protein to be particularly difficult to manage as most athletes get between 1.5-1.8gm/kg body mass. Time with a nutritionist can be helpful for the athlete to help formulate an individualized diet for their training schedule.
The nephropathy could also have been post traumatic with an intercurrent cellulitis or vasculitis with painful infarction involving the skin. Unlikely would also be lymphomatous involvement of the inguinal nodes with painful swelling.
It would be helpful to note the exact findings of the renal biopsy (mesangial, interstitial fibrosis or segmental disease) since the degree of renal injury can vary dramatically. Many "latent" IgA nephropathy patients exist with mild disease who are likely involved in contact sports.
MRI documentation of the cellulitis might also have been helpful since the US findings can be very nonspecific and lymphoma can be associated with IgA nephropathy.
What is the ethnicity of this patient? Clearly it would not change his diagnosis but IgA nephropathy is very rare in African Americans.
A discussion of the pericarditis in association with IgA nephropathy would also be interesting. It is unlikely that this was related to renal failure. Could it have been staphlococcal secondary to the cellulitis? Pericarditis is not associated with IgA nephropathy (as far as I can find) except in the setting of severe chronic renal failure. Was AC's MRSA screen positive or was any organism recovered.
Excellent case and summary.
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