American Journal of Therapeutics 23, e957–e960 (2016)
Unusual Cause and Presentation of Collapsing Focal Segmental Glomerulosclerosis Zeenat Yousuf Bhat, MD,* Neetu Sharma, MD, Unnikrishnana Pillai, MD, and Atul Singh, MD
Collapsing focal segmental glomerulosclerosis (c-FSGS), a structural variant of focal segmental glomeruloslecrosis (FSGS), is considered to be the most aggressive FSGS form. Most patients present with severe nephrotic syndrome and often have rapidly progressing renal failure and progression to end-stage kidney disease. We are reporting a 28-year-old previously healthy woman, who was started on griseofulvin for onchomycosis; she subsequently developed acute renal failure with significant proteinuria. Exposure to the drug caused dramatic decline in the renal function. Renal biopsy was compatible with c-FSGS. To the best of our knowledge, this is the first case of biopsy-proven griseofulvin-associated c-FSGS. Our patient showed rapid improvement in renal function after discontinuation of griseofulvin. Universally, c-FSGS carries poor prognosis, but this case is unique because patient showed rapid improvement in renal function with a short duration after cessation of griseofulvin. Keywords: collapsing focal segmental glomerulosclerosis, griseofulvin, acute kidney injury
INTRODUCTION Collapsing focal segmental glomerulosclerosis (c-FSGS) is considered to be the most aggressive form of FSGS.1,2 Commonly, patients present with nephrotic syndrome, and there is rapid decline in glomerular filtration rate and progression to end-stage kidney disease.3 Because of the rapidly progressive disease course, it was first described as “malignant focal segmental glomerulosclerosis.”4 c-FSGS was a common biopsy lesion of uncontrolled HIV infection during HIV pandemic in early 1980s. HIV-associated nephropathy was generally used to describe patients with similar histology.5,6 Often c-FSGS and HIV-associated nephropathy were used synonymously; however, afterward, similar renal lesion
Division of Nephrology, Department of Internal Medicine, Wayne State University—Detroit Medical Center, Detroit, MI. The authors have no conflicts of interest to declare. *Address for correspondence: Division of Nephrology, Department of Internal Medicine, Wayne State University, Detroit, MI. E-mail: [email protected]
in HIV-negative patients with severe proteinuria and rapid progression to renal failure were reported; “collapsing glomerulopathy” was coined for this new clinical pathologic entity.3 c-FSGS has been found to be associated with wide variety of clinical conditions like infections, autoimmune disorders, malignancies, genetic disorders, drug associated, and in renal transplant recipients,7–13 with near universal poor renal outcomes.
CASE DESCRIPTION A 28-year-old previously healthy African American woman admitted to the hospital with 3-day history of nausea and loose stools. She had ongoing severe fatigue and generalized body pain but no fever or chills. She had noticed rash over arms and thighs. She reported taking griseofulvin 500 mg per day for 14 days, which was prescribed to her for onychomycosis of the great toe. She completed the prescribed therapy 2 days before the presentation. She also admitted taking 2 dose of over the counter ibuprofen 200 mg, in the past 2 weeks. No other medication use. Medical history was
1075–2765 Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Bhat et al
e958 Table 1. Results of patient’s blood tests.*
Blood tests dsDNA ANA titer Rheumatoid factor C3, mg/dL C4, mg/dL CMV HAV, HBV, HCV, and HIV
Results Negative Weakly positive 7.5 167 37 Negative Negative
Normal values
0–6 90–200 16–50
*ANA, antinuclear antibodies; CMV, cytomegalovirus; EBV, Epstein–Barr virus; HSV, herpes simplex virus; HAV, hepatitis A virus.
significant for genital herpes simplex virus type 2 diagnosed few years ago with no recent flares. She was a medical unit–registered nurse. Her physical examination was unremarkable except mild tachycardia, and 2/6 ejection systolic flow murmur and bilateral maculopapular rash present anterior aspect of the legs. Examination was also compatible with anasarca. Laboratory data at the time of admission had a white blood cell count of 10.3 K/CUMM with 19% lymphocytes, 63% neutrophils, 15% monocytes, and 2% eosinophils along with mild thrombocytopenia of 147 K/CUMM. Serum creatinine was elevated at 2.8 mg/dL (baseline creatinine of 0.9 mg/ dL), and blood urea nitrogen value was 28 mg/dL. Urine analysis revealed specific gravity of 1.022, moderate proteinuria, 10–20 red blood cells per high power field, less than 5 white blood cells, and 2–5 hyaline casts. HIV and hepatitis B and C panel were negative. During the course of her hospital admission, her rash resolved along with improved of gastrointestinal symptoms. Despite this symptomatic improvement and adequate volume expansion, creatinine peaked at 3.9 mg/dL. Urine protein quantification showed 2569 mg/dL of proteins in the urine. Her albumin fell from 4.1 to 1.7 g/dL. Peripheral smear did not show any evidence of schistocytes. ADAMST3 antibodies
and C3, C4 complements were normal. Antinuclear antibodies came back weakly positive. Other serological tests are shown in Table 1. The patient underwent a renal biopsy. Two of twenty-four glomeruli seen showed collapsing of capillary tuft with podocyte hyperplasia. There was also diffuse and severe tubular injury and interstitial nephritis with clusters of eosinophils and intratubular neutrophils. Many proximal tubules contained protein resorption droplets and also flattening and simplification of tubular epithelium. Electron microscopy showed wrinkling and folding of glomerular basement membrane along with diffuse and complete podocyte foot processes effacement with microvillus changes (Figure 2). Immunofluorescence showed only traces of diffuse linear glomerular capillary IgG, albumin, kappa light chain, and lambda light chain deposits. No IgA, IgM, C3, or C1q was noted. There was no evidence of amyloidosis, myeloma cast nephropathy, or light chain deposit disease. During her hospital course, serum creatinine improved from peak of 3.9 mg/dL and then declined to 1.9 mg/dL (Figure 1A). With clinical and laboratory improvement, she was discharged home. The patient was seen in the clinic on follow-up. A month later, her creatinine has improved to 0.9 mg/dL with the decrease in proteinuria to 135 mg/dL (Figure 1B). Anasraca had resolved, and overall the patient was feeling well.
DISCUSSION Griseofulvin is an antifungal that is derived from several species of Penicillium and is used for the treatment of Tinea capitis (ringworm) and other dermatophyte infections. Most of the drugs (10%–50%) are excreted almost exclusively as metabolites in the urine. It is an antimitotic agent that selectively inhibits fungal cell mitosis in association with its accumulation in the keratin layers of the epidermis.14 Most common side effects of griseofulvin described are gastrointestinal disturbances such as nausea, vomiting, and diarrhea. Headache is also a relatively frequent side effect and is
FIGURE 1. Changes in serum creatinine with time (A) and changes in urine protein to urine creatinine (Up/UC) with time (B). American Journal of Therapeutics (2016) 23(3)
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Collapsing Focal Segmental Glomerulosclerosis
e959
FIGURE 2. (A) Silver stain showed collapsing of capillary tuft with podocyte hyperplasia. (B) Electron microscopy showing wrinkling and folding of glomerular basement membrane along with diffuse and complete podocyte foot processes effacement with microvillus changes.
not usually severe and is temporary. Other common side effects of this drug include photosensitivity, urticaria, and rash. Rarely life-threatening complications such as hepatotoxicity and severe immunologic and allergic phenomenon have been reported. Adverse hematological side effects are rare and include transient leucopenia and neutropenia. Literature review shows previous case reports of interstitial nephritis with albuminuria by griseofulvin and varied manifestation. A previous case report mentioned acute renal insufficiency and isolated erythroid hypoplasia caused by long-term use of griseofulvin, although renal biopsy was documented.15 Renal function and isolated erythroid hypoplasia normalized with discontinuation of the drug.15 Nephrotic syndrome related to systemic lupus erythematosus after griseofulvin therapy has been described. There is also a case of griseofulvin-induced acute glomerulonephritis that has been reported.16,17 There are no documented cases of c-FSGS. FSGS and c-FSGS have been well described with drugs. Bisphosphonates are used commonly; renal injury and c-FSGS have been described. The potential mechanism of renal toxicity of griseofulvin remains unclear.7 c-FSGS usually has a precipitous course and often patients progress to end stage renal disease. In 2 retrospective case series, patients with c-FSGS were more likely to be on renal replacement therapy within 15 months (5 of 14 compared with none of 25 with noncollapsing focal glomerulosclerosis).18 Median time to end stage renal disease was also shorter in c-FSGS versus controls (13.0 vs. 62.5 months, P , 0.05).2,8,19 c-FSGS is a histological diagnosis. Columbia classification scheme suggests that a collapsing lesion in 1 capillary loop is significant and diagnostic (response to medical therapy in c-FSGS in HIV-negative patients, unfortunately is dismal). Use of glucocorticoids and cutotoxic therapy with cyclophosphamide has been www.americantherapeutics.com
described with poor response. In 1 study, none of the 26 patients treated with glucocorticoids, and in 1 of 6 (partial remission) treated with cyclophosphamide8,9,18 showed response. In a second report of 23 patients, complete or partial remission was observed in 2 and 7 patients treated with glucocorticoids, respectively. Inhibition of cyclin-dependent kinases that control cell replication in renal epithelium and, inflammatory pathways that involve nuclear factor kappa-light-chainenhancer of activated B cells and cyclooxygenase-2 also have shown some promise in experimental c-FSGS.9,19,20 Steroids can be used for such an effect, but the clinical reports so far are not as promising. Our patient was not treated with steroids, as she declined the medication given its side effect profile. Spontaneous remission and clinical improvement were unusual in her presentation. Near-complete clinical renal recovery was present. No repeat histology was performed, but her renal function was stable on long term despite no renal directed therapy. Improvement seen in this patient after discontinuation of drug is unusual presentation of c-FSGS, which makes this case very unique.
CONCLUSIONS Physicians should be aware of the possibility of c-FSGS and acute interstitial nephritis being rare adverse effects of griseofulvin, and use caution while prescribing these drugs (especially in combination of nonsteroidal anti-inflammatory drugs). Griseofulvin has often been treated as an innocuous drug, but physicians should monitor the patients on griseofulvin for signs and symptoms of nephrotoxicity including a urine analysis, renal function, and consider alternative therapy if there are even low grades of urine protein losses. American Journal of Therapeutics (2016) 23(3)
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
e960
REFERENCES 1. D’Agati V. Pathologic classification of focal segmental glomerulosclerosis. Semin Nephrol. 2003;23:117. 2. Detwiler RK, Falk RJ, Hogan SL, et al. Collapsing glomerulopathy: a clinically and pathologically distinct variant of focal segmental glomerulosclerosis. Kidney Int. 1994;45: 1416–1424. 3. Weiss MA, Daquioag E, Margolin EG, et al. Nephrotic syndrome, progressive irreversible renal failure, and glomerular “collapse”: a new clinicopathologic entity. Am J Kidney Dis. 1986;7:20–28. 4. Albaqumi M, Soos TJ, Barisoni L, et al. Collapsing glomerulopathy. J Am Soc Nephrol. 2006;17:2854–2863. 5. Humphreys MH. Human immunodeficiency virusassociated glomerulosclerosis. Kidney Int. 1995;48:311. 6. D’Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol. 1997;8:138. 7. Markowitz GS, Appel GB, Fine PL, et al. Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate. J Am Soc Nephrol. 2001;12: 1164–1172. 8. Valeri A, Barisoni L, Appel GB, et al. Idiopathic collapsing focal segmental glomerulosclerosis: a clinicopathologic study. Kidney Int. 1996;50:1734–1746. 9. Laurinavicius A, Hurwitz S, Rennke HG. Collapsing glomerulopathy in HIV and non-HIV patients: a clinicopathological and follow-up study. Kidney Int. 1999;56:2203–2213. 10. Stein DF, Ahmed A, Sunkhara V, et al. Collapsing focal segmental glomerulosclerosis with recovery of renal function: an uncommon complication of interferon therapy for hepatitis C. Dig Dis Sci. 2001;46:530–535.
American Journal of Therapeutics (2016) 23(3)
Bhat et al 11. Clarkson MR, O’Meara YM, Murphy B, et al. Collapsing glomerulopathy: recurrence in a renal allograft. Nephrol Dial Transpl. 1998;13:503–506. 12. Toth CM, Pascual M, Williams WW Jr, et al. Recurrent collapsing glomerulopathy. Transplantation. 1998;65:1009–1010. 13. Badhwar A, Berkovic SF, Dowling JP, et al. Action myoclonus-renal failure syndrome: characterization of a unique cerebro-renal disorder. Brain. 2004;127:2173– 2182. 14. Panda D, Rathinasamy K, Santra MK, et al. Kinetic suppression of microtubule dynamic instability by griseofulvin: implications for its possible use in the treatment of cancer. Proc Natl Acad Sci USA. 2005;102:9878–9883. 15. Haskell LP, Mennemyer RP, Greenman R, et al. Isolated erythroid hypoplasia and renal insufficiency induced by long term treatment of griseofulvin therapy. South Med J. 1990;83:1327–1330. 16. Bonilla-Felix M, Verani R, Vanasse LG, et al. Nephrotic syndrome related to systemic lupus erythematosus after griseofulvin therapy. Pediatr Nephrol. 1995;9:478–479. 17. Narahari SR. Griseofulvin-induced acute glomerulonephritis. Indian J Dermatol Venereol Leprol. 1996;62:335. 18. Nelson PJ, D’Agati VD, Gries JM, et al. Amelioration of nephropathy in mice expressing HIV-1 genes by the cyclin-dependent kinase inhibitor flavopiridol. J Antimicrob Chemother. 2003;51:921–929. 19. Grcevska L, Polenakovik M. Collapsing glomerulopathy: clinical characteristics and follow-up. Am J Kidney Dis. 1999;33:652. 20. Hermann M, Shaw S, Kiss E, et al. Selective COX-2 inhibitors and renal injury in salt-sensitive hypertension. Hypertension. 2005;45:193–197.
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Unusual Cause and Presentation of Collapsing Focal Segmental Glomerulosclerosis Zeenat Yousuf Bhat, MD,* Neetu Sharma, MD, Unnikrishnana Pillai, MD, and Atul Singh, MD
Collapsing focal segmental glomerulosclerosis (c-FSGS), a structural variant of focal segmental glomeruloslecrosis (FSGS), is considered to be the most aggressive FSGS form. Most patients present with severe nephrotic syndrome and often have rapidly progressing renal failure and progression to end-stage kidney disease. We are reporting a 28-year-old previously healthy woman, who was started on griseofulvin for onchomycosis; she subsequently developed acute renal failure with significant proteinuria. Exposure to the drug caused dramatic decline in the renal function. Renal biopsy was compatible with c-FSGS. To the best of our knowledge, this is the first case of biopsy-proven griseofulvin-associated c-FSGS. Our patient showed rapid improvement in renal function after discontinuation of griseofulvin. Universally, c-FSGS carries poor prognosis, but this case is unique because patient showed rapid improvement in renal function with a short duration after cessation of griseofulvin. Keywords: collapsing focal segmental glomerulosclerosis, griseofulvin, acute kidney injury
INTRODUCTION Collapsing focal segmental glomerulosclerosis (c-FSGS) is considered to be the most aggressive form of FSGS.1,2 Commonly, patients present with nephrotic syndrome, and there is rapid decline in glomerular filtration rate and progression to end-stage kidney disease.3 Because of the rapidly progressive disease course, it was first described as “malignant focal segmental glomerulosclerosis.”4 c-FSGS was a common biopsy lesion of uncontrolled HIV infection during HIV pandemic in early 1980s. HIV-associated nephropathy was generally used to describe patients with similar histology.5,6 Often c-FSGS and HIV-associated nephropathy were used synonymously; however, afterward, similar renal lesion
Division of Nephrology, Department of Internal Medicine, Wayne State University—Detroit Medical Center, Detroit, MI. The authors have no conflicts of interest to declare. *Address for correspondence: Division of Nephrology, Department of Internal Medicine, Wayne State University, Detroit, MI. E-mail: [email protected]
in HIV-negative patients with severe proteinuria and rapid progression to renal failure were reported; “collapsing glomerulopathy” was coined for this new clinical pathologic entity.3 c-FSGS has been found to be associated with wide variety of clinical conditions like infections, autoimmune disorders, malignancies, genetic disorders, drug associated, and in renal transplant recipients,7–13 with near universal poor renal outcomes.
CASE DESCRIPTION A 28-year-old previously healthy African American woman admitted to the hospital with 3-day history of nausea and loose stools. She had ongoing severe fatigue and generalized body pain but no fever or chills. She had noticed rash over arms and thighs. She reported taking griseofulvin 500 mg per day for 14 days, which was prescribed to her for onychomycosis of the great toe. She completed the prescribed therapy 2 days before the presentation. She also admitted taking 2 dose of over the counter ibuprofen 200 mg, in the past 2 weeks. No other medication use. Medical history was
1075–2765 Copyright © 2014 Wolters Kluwer Health, Inc. All rights reserved.
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Bhat et al
e958 Table 1. Results of patient’s blood tests.*
Blood tests dsDNA ANA titer Rheumatoid factor C3, mg/dL C4, mg/dL CMV HAV, HBV, HCV, and HIV
Results Negative Weakly positive 7.5 167 37 Negative Negative
Normal values
0–6 90–200 16–50
*ANA, antinuclear antibodies; CMV, cytomegalovirus; EBV, Epstein–Barr virus; HSV, herpes simplex virus; HAV, hepatitis A virus.
significant for genital herpes simplex virus type 2 diagnosed few years ago with no recent flares. She was a medical unit–registered nurse. Her physical examination was unremarkable except mild tachycardia, and 2/6 ejection systolic flow murmur and bilateral maculopapular rash present anterior aspect of the legs. Examination was also compatible with anasarca. Laboratory data at the time of admission had a white blood cell count of 10.3 K/CUMM with 19% lymphocytes, 63% neutrophils, 15% monocytes, and 2% eosinophils along with mild thrombocytopenia of 147 K/CUMM. Serum creatinine was elevated at 2.8 mg/dL (baseline creatinine of 0.9 mg/ dL), and blood urea nitrogen value was 28 mg/dL. Urine analysis revealed specific gravity of 1.022, moderate proteinuria, 10–20 red blood cells per high power field, less than 5 white blood cells, and 2–5 hyaline casts. HIV and hepatitis B and C panel were negative. During the course of her hospital admission, her rash resolved along with improved of gastrointestinal symptoms. Despite this symptomatic improvement and adequate volume expansion, creatinine peaked at 3.9 mg/dL. Urine protein quantification showed 2569 mg/dL of proteins in the urine. Her albumin fell from 4.1 to 1.7 g/dL. Peripheral smear did not show any evidence of schistocytes. ADAMST3 antibodies
and C3, C4 complements were normal. Antinuclear antibodies came back weakly positive. Other serological tests are shown in Table 1. The patient underwent a renal biopsy. Two of twenty-four glomeruli seen showed collapsing of capillary tuft with podocyte hyperplasia. There was also diffuse and severe tubular injury and interstitial nephritis with clusters of eosinophils and intratubular neutrophils. Many proximal tubules contained protein resorption droplets and also flattening and simplification of tubular epithelium. Electron microscopy showed wrinkling and folding of glomerular basement membrane along with diffuse and complete podocyte foot processes effacement with microvillus changes (Figure 2). Immunofluorescence showed only traces of diffuse linear glomerular capillary IgG, albumin, kappa light chain, and lambda light chain deposits. No IgA, IgM, C3, or C1q was noted. There was no evidence of amyloidosis, myeloma cast nephropathy, or light chain deposit disease. During her hospital course, serum creatinine improved from peak of 3.9 mg/dL and then declined to 1.9 mg/dL (Figure 1A). With clinical and laboratory improvement, she was discharged home. The patient was seen in the clinic on follow-up. A month later, her creatinine has improved to 0.9 mg/dL with the decrease in proteinuria to 135 mg/dL (Figure 1B). Anasraca had resolved, and overall the patient was feeling well.
DISCUSSION Griseofulvin is an antifungal that is derived from several species of Penicillium and is used for the treatment of Tinea capitis (ringworm) and other dermatophyte infections. Most of the drugs (10%–50%) are excreted almost exclusively as metabolites in the urine. It is an antimitotic agent that selectively inhibits fungal cell mitosis in association with its accumulation in the keratin layers of the epidermis.14 Most common side effects of griseofulvin described are gastrointestinal disturbances such as nausea, vomiting, and diarrhea. Headache is also a relatively frequent side effect and is
FIGURE 1. Changes in serum creatinine with time (A) and changes in urine protein to urine creatinine (Up/UC) with time (B). American Journal of Therapeutics (2016) 23(3)
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
Collapsing Focal Segmental Glomerulosclerosis
e959
FIGURE 2. (A) Silver stain showed collapsing of capillary tuft with podocyte hyperplasia. (B) Electron microscopy showing wrinkling and folding of glomerular basement membrane along with diffuse and complete podocyte foot processes effacement with microvillus changes.
not usually severe and is temporary. Other common side effects of this drug include photosensitivity, urticaria, and rash. Rarely life-threatening complications such as hepatotoxicity and severe immunologic and allergic phenomenon have been reported. Adverse hematological side effects are rare and include transient leucopenia and neutropenia. Literature review shows previous case reports of interstitial nephritis with albuminuria by griseofulvin and varied manifestation. A previous case report mentioned acute renal insufficiency and isolated erythroid hypoplasia caused by long-term use of griseofulvin, although renal biopsy was documented.15 Renal function and isolated erythroid hypoplasia normalized with discontinuation of the drug.15 Nephrotic syndrome related to systemic lupus erythematosus after griseofulvin therapy has been described. There is also a case of griseofulvin-induced acute glomerulonephritis that has been reported.16,17 There are no documented cases of c-FSGS. FSGS and c-FSGS have been well described with drugs. Bisphosphonates are used commonly; renal injury and c-FSGS have been described. The potential mechanism of renal toxicity of griseofulvin remains unclear.7 c-FSGS usually has a precipitous course and often patients progress to end stage renal disease. In 2 retrospective case series, patients with c-FSGS were more likely to be on renal replacement therapy within 15 months (5 of 14 compared with none of 25 with noncollapsing focal glomerulosclerosis).18 Median time to end stage renal disease was also shorter in c-FSGS versus controls (13.0 vs. 62.5 months, P , 0.05).2,8,19 c-FSGS is a histological diagnosis. Columbia classification scheme suggests that a collapsing lesion in 1 capillary loop is significant and diagnostic (response to medical therapy in c-FSGS in HIV-negative patients, unfortunately is dismal). Use of glucocorticoids and cutotoxic therapy with cyclophosphamide has been www.americantherapeutics.com
described with poor response. In 1 study, none of the 26 patients treated with glucocorticoids, and in 1 of 6 (partial remission) treated with cyclophosphamide8,9,18 showed response. In a second report of 23 patients, complete or partial remission was observed in 2 and 7 patients treated with glucocorticoids, respectively. Inhibition of cyclin-dependent kinases that control cell replication in renal epithelium and, inflammatory pathways that involve nuclear factor kappa-light-chainenhancer of activated B cells and cyclooxygenase-2 also have shown some promise in experimental c-FSGS.9,19,20 Steroids can be used for such an effect, but the clinical reports so far are not as promising. Our patient was not treated with steroids, as she declined the medication given its side effect profile. Spontaneous remission and clinical improvement were unusual in her presentation. Near-complete clinical renal recovery was present. No repeat histology was performed, but her renal function was stable on long term despite no renal directed therapy. Improvement seen in this patient after discontinuation of drug is unusual presentation of c-FSGS, which makes this case very unique.
CONCLUSIONS Physicians should be aware of the possibility of c-FSGS and acute interstitial nephritis being rare adverse effects of griseofulvin, and use caution while prescribing these drugs (especially in combination of nonsteroidal anti-inflammatory drugs). Griseofulvin has often been treated as an innocuous drug, but physicians should monitor the patients on griseofulvin for signs and symptoms of nephrotoxicity including a urine analysis, renal function, and consider alternative therapy if there are even low grades of urine protein losses. American Journal of Therapeutics (2016) 23(3)
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
e960
REFERENCES 1. D’Agati V. Pathologic classification of focal segmental glomerulosclerosis. Semin Nephrol. 2003;23:117. 2. Detwiler RK, Falk RJ, Hogan SL, et al. Collapsing glomerulopathy: a clinically and pathologically distinct variant of focal segmental glomerulosclerosis. Kidney Int. 1994;45: 1416–1424. 3. Weiss MA, Daquioag E, Margolin EG, et al. Nephrotic syndrome, progressive irreversible renal failure, and glomerular “collapse”: a new clinicopathologic entity. Am J Kidney Dis. 1986;7:20–28. 4. Albaqumi M, Soos TJ, Barisoni L, et al. Collapsing glomerulopathy. J Am Soc Nephrol. 2006;17:2854–2863. 5. Humphreys MH. Human immunodeficiency virusassociated glomerulosclerosis. Kidney Int. 1995;48:311. 6. D’Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol. 1997;8:138. 7. Markowitz GS, Appel GB, Fine PL, et al. Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate. J Am Soc Nephrol. 2001;12: 1164–1172. 8. Valeri A, Barisoni L, Appel GB, et al. Idiopathic collapsing focal segmental glomerulosclerosis: a clinicopathologic study. Kidney Int. 1996;50:1734–1746. 9. Laurinavicius A, Hurwitz S, Rennke HG. Collapsing glomerulopathy in HIV and non-HIV patients: a clinicopathological and follow-up study. Kidney Int. 1999;56:2203–2213. 10. Stein DF, Ahmed A, Sunkhara V, et al. Collapsing focal segmental glomerulosclerosis with recovery of renal function: an uncommon complication of interferon therapy for hepatitis C. Dig Dis Sci. 2001;46:530–535.
American Journal of Therapeutics (2016) 23(3)
Bhat et al 11. Clarkson MR, O’Meara YM, Murphy B, et al. Collapsing glomerulopathy: recurrence in a renal allograft. Nephrol Dial Transpl. 1998;13:503–506. 12. Toth CM, Pascual M, Williams WW Jr, et al. Recurrent collapsing glomerulopathy. Transplantation. 1998;65:1009–1010. 13. Badhwar A, Berkovic SF, Dowling JP, et al. Action myoclonus-renal failure syndrome: characterization of a unique cerebro-renal disorder. Brain. 2004;127:2173– 2182. 14. Panda D, Rathinasamy K, Santra MK, et al. Kinetic suppression of microtubule dynamic instability by griseofulvin: implications for its possible use in the treatment of cancer. Proc Natl Acad Sci USA. 2005;102:9878–9883. 15. Haskell LP, Mennemyer RP, Greenman R, et al. Isolated erythroid hypoplasia and renal insufficiency induced by long term treatment of griseofulvin therapy. South Med J. 1990;83:1327–1330. 16. Bonilla-Felix M, Verani R, Vanasse LG, et al. Nephrotic syndrome related to systemic lupus erythematosus after griseofulvin therapy. Pediatr Nephrol. 1995;9:478–479. 17. Narahari SR. Griseofulvin-induced acute glomerulonephritis. Indian J Dermatol Venereol Leprol. 1996;62:335. 18. Nelson PJ, D’Agati VD, Gries JM, et al. Amelioration of nephropathy in mice expressing HIV-1 genes by the cyclin-dependent kinase inhibitor flavopiridol. J Antimicrob Chemother. 2003;51:921–929. 19. Grcevska L, Polenakovik M. Collapsing glomerulopathy: clinical characteristics and follow-up. Am J Kidney Dis. 1999;33:652. 20. Hermann M, Shaw S, Kiss E, et al. Selective COX-2 inhibitors and renal injury in salt-sensitive hypertension. Hypertension. 2005;45:193–197.
www.americantherapeutics.com
Copyright © 2014 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited.
