- Email: [email protected]
Fibrillary glomerulonephritis and Charcot-Marie-Tooth disease
CASE REPORT
Fibrillary Glomerulonephritis and Charcot-Marie-Tooth Disease Miguel A. Nadal, MD, Nestor R. Lago, MD, Liliana E. Olivieri, MD, Graciela de Rosa, MD, and Tomas Pierri, MD ● We report the case of a young white man with Charcot-Marie-Tooth disease type 1 that began at 4 years. At 15 years, he developed proteinuria, arterial hypertension, and renal insufficiency. Renal biopsy specimens studied by electron microscopy showed deposition of nonamyloidotic microfibrils. This is the first report of fibrillary glomerulopathy associated with this neurological disorder. r 1998 by the National Kidney Foundation, Inc. INDEX WORDS: Fibrillary glomerulonephritis; immunotactoid glomerulopathy; Charcot-Marie-Tooth disease; nephrotic syndrome.
F
IBRILLARY glomerulonephritis (FG) is an apparent primary glomerulopathy characterized by proteinuria, which is often in nephrotic range, microscopic hematuria, arterial hypertension, and possible progression to renal insufficiency.1,2 Conversely, Charcot-Marie-Tooth disease (CMT) is an inheritable disorder of peripheral nerves in which focal glomerulosclerosis occasionally has been described.3 However, we wish to comunicate the current case because it has shown the association of both FG and CMT. Such a combination has never been published before, at least in the bibliography within our reach. CASE REPORT A 15-year-old white boy was admitted to our Hospital in March 1995 for the evaluation of proteinuria and renal insufficiency. The patient’s parents do not suffer from any evident neurological or nephrological disease. In 1984, at 4 years of age, he began to experience some difficulty walking and frequent episodes of bilateral foot drop. The neurological examination discovered muscular atrophy in the lower limbs (calves and feet), aquilian areflexia but without any sensory alterations, and bilateral equinovarus. External popliteal nerve and posterior tibial nerve electromyographies showed peripheral neuropathy of the multiple axonal and demyelinating types. A neuromuscular biopsy specimen of external saphenous nerve, studied by electron microscopy, showed a severe demyelination and remyelination process with formation of onion bulbs, all of which led to a CMT diagnosis. This was later confirmed by finding duplication on chromosome 17* (CMT type 1 disease). In the following years, no other evidence of clinical alterations were detected. In
*This study was carried out in August 1995 in The Center for Human Genetics, Boston University School of Medicine.
January 1995, when the patient was 15 years old, he reported experiencing nocturia. His blood pressure was 160/100 mm Hg, and he was treated with enalapril, 2.5 mg/day, and a low-protein diet. The analysis results were as follows: blood urea, 18.5 mmol/L (52 mg/dL); creatinine, 203 µmol/L (2.3 mg/dL); hematocrit, 42%; hemoglobin, 13.5 g/dL; red blood cells, 4,400,000/mm3; white blood cells, 7,400 mm3; erythrocyte sedimentation rate, 11 mm/h. The following tests were negative: Venereal Disease Research Laboratory, lupus erythematosus cell test, antinuclear antibodies, anti-DNA, rheumatoid factor, cryoglobulin, and hepatitis B surface antigen. Total hemolytic complement was 32 mg/dL; C3, 93 mg/dL; C4, 25 mg/dL; total serum protein, 6 g/dL; (albumin, 3.4 g/dL; globulins, 2.6 g/dL). Serum and urine immunoelectrophoresis for free monoclonal light chains and urine immunofixation for beta-2microglobulin were negative. In March 1995, urinalysis gave the following results: specific gravity, 1,010; pH 5.5; proteinuria, ⫹⫹⫹; white blood cells, 12 to 15 per high-power field; red blood cells, 20 to 30 per high-power field; granular and fatty casts and proteinuria, 4 g/d. Urinary protein electrophoresis showed a nonselective glomerular pattern. On the same date, a percutaneous renal biopsy was performed. The specimen for light microscopy contained 30 glomeruli, of which 21 were globally sclerotic and four segmentally sclerotic with mesangial hypercellularity associated. The remnant five glomeruli showed mesangial matrix expansion. In addition, crescents were observed in four glomeruli (Fig 1). Moderate tubular atrophy, interstitial fibrosis, and edema were present, as well as focal nonspecific inflammatory infiltrate.
From the Department of Pathology and the Nephrology Division, Hospital de Clinicas, Buenos Aires University, Argentina. Received November 3, 1997; accepted in revised form July 24, 1998. Address reprint requests to Miguel A. Nadal, MD, Hospital de Clinicas, Division Nefrologia, Av. Cordoba 2351 CP 1120, Buenos Aires, Argentina. E-mail: [email protected]
r 1998 by the National Kidney Foundation, Inc. 0272-6386/98/3205-0027$3.00/0
American Journal of Kidney Diseases, Vol 32, No 5 (November), 1998: E3
1
2
NADAL ET AL
Fig 1. Fibrous crescent with disruption of Bowman’s capsule, glomerular tuft collapse, and segmental sclerosis (PAS, original magnification ⴛ200).
The arterioles and small and medium-sized arteries were normal. Fluorescence microscopy disclosed 2 to 3⫹ segmental to global coarse granular deposits in isolated glomerular capillary walls and also mesangium of immunoglobulin (Ig) M, C1q, and C3, whereas IgG, IgA, and fibrinogen were negative. The deposits in the capillary wall and mesangial matrix were Congo red negative and thioflavine-T negative. Electron microscopy of nonsclerosed glomeruli showed mesangial expansion and widening of the basement membranes of glomerular capillaries. Granular and fibrillary nonbranching deposits were observed in subendothelial and mesangial areas. The fibrils were randomly arranged and had a diameter slightly larger than amyloid fibrils (Fig 2). The final histological diagnosis was fibrillary glomerulonephritis. The patient continued with restrictions of salt and protein in his diet, and his blood pressure was normalized, changing enalapril for nifedipine. In December 1995, he showed uremic syndrome with blood urea of 88.5 mmol/L (248 mg/dL); creatinine, 778 µmol/L (8.8 mg/dL); and endogenous creatinine clearance of 8.8 mL/min, and he started hemodialysis.
More than 12 patients have been reported in the literature with the association of CMT and glomerulopathies. Moreover, Gherardi et al3 and Denian et al6 concluded that focal segmental glomerulosclerosis was the morphological lesion found in all reported patients with CMT. However, a case of immune complex glomerulonephritis in a patient with CMT also has been described.7 In addition, Paul et al8 described two patients (mother and daughter) who had CMT associated with renal involvement. The child was studied with renal biopsy and showed, in electron microscopy, thinning and splitting of the basement membrane as in Alport disease. No fibrillary deposits were found. Renal biopsy was not performed on the mother. The pattern and distribution of the deposits in immunofluorescence microscopy in our patient suggest the possibility of IgM, C1q, and C3 trapping in the widened mesangium, sparce capillary walls, and sclerotic areas. These findings seem to be similar to other, previously reported cases of CMT associated with focal and segmental glomerulosclerosis.8
DISCUSSION
In this patient, the diagnosis of hereditary peripheral neuropathy of CMT type 1 was made on the basis of the insidious onset of distal muscle weakness and wasting in the lower limbs, areflexia at the ankles, evidence of demyelinating neuropathy on motor nerve conduction studies, and duplication of chromosome 17, which encodes the peripheral myelin protein 22 gene.4 CMT is usually transmited by autosomal dominant inheritance, but an autosomal recessive pattern also has been described. The absence of neurological disorders in our patient’s parents is more compatible with a recessive autosomic variant.5
Fig 2. Electron micrograph shows randomly arranged microfibrils in the subendothelial space of the glomerular capillary (Original magnification ⴛ30,000).
FIBRILLARY AND CHARCOT-MARIE-TOOTH DISEASE
3
Conversely, deposits of IgG and C3 have been found in many cases of FG. However, they were scant or negative in our patients, as they were in some of the reported cases with FG. This might be attributed to the advanced sclerosing stage present in this biopsy specimen. Electron microscopy of renal tissue was performed in five of these cases with CMT, and no fibrillary deposits were shown.3,6,8-10 However, we cannot exclude some other case of FG among those patients who were not studied by electron microscopy. FG is an unusual primary kidney disease,11 characterized by deposition of immunoglobulins in a fibrillar pattern that resembles amyloid but does not stain with Congo red. In a report of a series of patients with this glomerulopathy, Duffy et al12 used the term fibrillary to describe the characteristic ultrastructure of the immune deposits. After this, Alpers et al13 proposed the name FG for this disease. The case described in our report had the typical clinical manifestations of FG, such as heavy proteinuria, arterial hypertension, and progressive renal insufficiency, and it lacked evidence of systemic lupus erythematosus, cryoglobulinemia, amyloidosis, or light chain deposition disease. The patients’ age at discovery of FG is frequently between 40 and 50 years, but typical cases have been reported in patients from 10 to 80 years of age,14 as in our young patient. On electron microscopy, the renal biopsy specimen showed the fibrillar deposits that were randomly oriented and located in the mesangial matrix and the endothelial side of the glomerular basement membrane. This finding has been essential for the diagnosis of FG. FG is pathologically characterized by fibrillar deposits that can be 10 to 30 nm in diameter. There is a debate about whether FG differs from the so-called immunotactoid glomerulopathy, in which microtubular structures ranging from 18 to 90 nm in diameter are seen. The question must await further study.15,16 Although recent reviews of FG have emphasized a lack of extrarenal manifestations, some data suggest that these patients infrequently can show involvement in other organs.17,18
Furthermore, the association of FG with other conditions has been reported.19-24 Because FG is an entity of uncertain origin and pathogenesis, and CMT is a genetic abnormality, we think that the juxtaposition of both diseases could be considered merely fortituous. This case of FG is remarkable because we have not found any prior description of its association with CMT in the literature. REFERENCES 1. Rosenmann E, Eliakim M: Nephrotic syndrome associated with amyloid-like glomerular deposits. Nephron 18:301308, 1997 2. Panner BJ: Rapidly progressive glomerulonephritis and possible amyloidosis. Arch Pathol Lab Med 104:603609, 1980 3. Gherardi R, Beighti-Deprez D, Hirbec G, Bouche P, Weil B, Lagrue G: Focal glomerulosclerosis associated with Charcot-Marie-Tooth disease. Nephron 40:357-361, 1985 4. Lebo RV, Martelli L, Su Y, Li L, Lynch E, Mansfield E, Pua KH, Watson DF, Chue J, Hurko O: Prenatal diagnosis of Charcot-Marie-Tooth disease type 1A by multicolor in situ hybridization. Am J Med Genet 47:441-450, 1993 5. Ionasescu V, Zellweger H: Genetics in neurology, pp 374-392. New York, NY, Raven Press, 1983 6. Deniau F, Guillot M, Plus A, et al: Maladie de CharcotMarie-Tooth et ne´phropatie glomerulaire. Arch Fr Pediatr 43:791-793, 1986 7. Yudis M, Sirota RA: Immune complex glomerulonephritis in Charcot-Marie-Tooth disease. Am Soc Nephrol p 48A, 1982 (abstr) 8. Paul MD, Fernandez D, Pryse-Phillis W, et al: CharcotMarie-Tooth disease and nephropathy in a mother and daughter with a review of the literature. Nephron 54:80-85, 1990 9. Hara M, Ichida F, Higuchi A, et al: Nephropathy associated with Charcot-Marie-Tooth disease. Int J Pediatr Nephrol 5:99-102, 1984 10. Lloveras JJ: Focal glomerulosclerosis and CharcotMarie-Tooth disease, not a chance association? Nephron 43:231, 1986 11. Iskandar SS, Falk RJ, Charles Jennette J: Clinical and pathologic features of fibrillary glomerulonephritis. Kidney Int 42:1401-1407, 1992 12. Duffy L, Khurana E, Susin M, et al: Fibrillary renal deposits and nephritis. Am J Pathol 113:279-290, 1983 13. Alpers CE, Rennke HG, Hooper J Jr, et al: Fibrillary glomerulonephritis: An entity with unusual immunofluorescence features. Kidney Int 31:781-789, 1997 14. Korbet SM, Schwartz M: Immunotactoic glomerulopathy. Am J Kidney Dis 17:247-257, 1991 15. Alpers CE: Fibrillary glomerulonephritis and immunotactoid glomerulopathy: Two entities, not one. Am J Kidney Dis 22:448-451, 1993 16. Schwartz MM: Immunotactoid glomerulopathy: The case for Occam’s Razor. Am J Kidney Dis 22:446-447, 1993 17. Masson RG, Rennke HG, Gottieb MN: Pulmonary hemorrage in a patient with fibrillary glomerulonephritis. N Engl J Med 326:36-39, 1992
4
18. Ozawa K, Yamabe H, Fukushi K, et al: Case report of amyloid-like glomerulopathy with hepatic involvement. Nephron 58:347-350, 1991 19. Kohan DE, Perkins SL, Terreros DA: Immune complex glomerulonephritis with unusual microfibrilar deposits associated with primary bone marrow lymphoma. Am J Kidney Dis 21:47-51, 1993 20. Orfila C, Meeus F, Bernadet P, et al: Immunotactoid glomerulopathy and cutaneous vasculitis. Am J Nephrol 11:67-72, 1991 21. Schifferli JA, Merot Y, Cruchaud A, et al: Immunotactoid glomerulopathy with leucocytoclastic skin vasculitis
NADAL ET AL
and hypocomplementemia: A case report. Clin Nephrol 27:151-155, 1987 22. Rosenmann E, Brisson ML, Bercovitch DD, et al: Atypical membranous glomerulonephritis with fibrillar subepithelial deposits in a patient with malignant lymphoma. Nephron 48:226-230, 1988 23. Abraham G, Bargam JM, Blake PG, et al: Fibrillary glomerulonephritis in a patient with metastatic carcinoma of the liver. Am J Nephrol 10:251-254, 1990 24. Alonso R, Novoa D, Alonso MC, et al: Nonamyloidotic fibrillar glomerulopathy and rheumatoid arthritis. Nephron 63:120-121, 1993
Fibrillary Glomerulonephritis and Charcot-Marie-Tooth Disease Miguel A. Nadal, MD, Nestor R. Lago, MD, Liliana E. Olivieri, MD, Graciela de Rosa, MD, and Tomas Pierri, MD ● We report the case of a young white man with Charcot-Marie-Tooth disease type 1 that began at 4 years. At 15 years, he developed proteinuria, arterial hypertension, and renal insufficiency. Renal biopsy specimens studied by electron microscopy showed deposition of nonamyloidotic microfibrils. This is the first report of fibrillary glomerulopathy associated with this neurological disorder. r 1998 by the National Kidney Foundation, Inc. INDEX WORDS: Fibrillary glomerulonephritis; immunotactoid glomerulopathy; Charcot-Marie-Tooth disease; nephrotic syndrome.
F
IBRILLARY glomerulonephritis (FG) is an apparent primary glomerulopathy characterized by proteinuria, which is often in nephrotic range, microscopic hematuria, arterial hypertension, and possible progression to renal insufficiency.1,2 Conversely, Charcot-Marie-Tooth disease (CMT) is an inheritable disorder of peripheral nerves in which focal glomerulosclerosis occasionally has been described.3 However, we wish to comunicate the current case because it has shown the association of both FG and CMT. Such a combination has never been published before, at least in the bibliography within our reach. CASE REPORT A 15-year-old white boy was admitted to our Hospital in March 1995 for the evaluation of proteinuria and renal insufficiency. The patient’s parents do not suffer from any evident neurological or nephrological disease. In 1984, at 4 years of age, he began to experience some difficulty walking and frequent episodes of bilateral foot drop. The neurological examination discovered muscular atrophy in the lower limbs (calves and feet), aquilian areflexia but without any sensory alterations, and bilateral equinovarus. External popliteal nerve and posterior tibial nerve electromyographies showed peripheral neuropathy of the multiple axonal and demyelinating types. A neuromuscular biopsy specimen of external saphenous nerve, studied by electron microscopy, showed a severe demyelination and remyelination process with formation of onion bulbs, all of which led to a CMT diagnosis. This was later confirmed by finding duplication on chromosome 17* (CMT type 1 disease). In the following years, no other evidence of clinical alterations were detected. In
*This study was carried out in August 1995 in The Center for Human Genetics, Boston University School of Medicine.
January 1995, when the patient was 15 years old, he reported experiencing nocturia. His blood pressure was 160/100 mm Hg, and he was treated with enalapril, 2.5 mg/day, and a low-protein diet. The analysis results were as follows: blood urea, 18.5 mmol/L (52 mg/dL); creatinine, 203 µmol/L (2.3 mg/dL); hematocrit, 42%; hemoglobin, 13.5 g/dL; red blood cells, 4,400,000/mm3; white blood cells, 7,400 mm3; erythrocyte sedimentation rate, 11 mm/h. The following tests were negative: Venereal Disease Research Laboratory, lupus erythematosus cell test, antinuclear antibodies, anti-DNA, rheumatoid factor, cryoglobulin, and hepatitis B surface antigen. Total hemolytic complement was 32 mg/dL; C3, 93 mg/dL; C4, 25 mg/dL; total serum protein, 6 g/dL; (albumin, 3.4 g/dL; globulins, 2.6 g/dL). Serum and urine immunoelectrophoresis for free monoclonal light chains and urine immunofixation for beta-2microglobulin were negative. In March 1995, urinalysis gave the following results: specific gravity, 1,010; pH 5.5; proteinuria, ⫹⫹⫹; white blood cells, 12 to 15 per high-power field; red blood cells, 20 to 30 per high-power field; granular and fatty casts and proteinuria, 4 g/d. Urinary protein electrophoresis showed a nonselective glomerular pattern. On the same date, a percutaneous renal biopsy was performed. The specimen for light microscopy contained 30 glomeruli, of which 21 were globally sclerotic and four segmentally sclerotic with mesangial hypercellularity associated. The remnant five glomeruli showed mesangial matrix expansion. In addition, crescents were observed in four glomeruli (Fig 1). Moderate tubular atrophy, interstitial fibrosis, and edema were present, as well as focal nonspecific inflammatory infiltrate.
From the Department of Pathology and the Nephrology Division, Hospital de Clinicas, Buenos Aires University, Argentina. Received November 3, 1997; accepted in revised form July 24, 1998. Address reprint requests to Miguel A. Nadal, MD, Hospital de Clinicas, Division Nefrologia, Av. Cordoba 2351 CP 1120, Buenos Aires, Argentina. E-mail: [email protected]
r 1998 by the National Kidney Foundation, Inc. 0272-6386/98/3205-0027$3.00/0
American Journal of Kidney Diseases, Vol 32, No 5 (November), 1998: E3
1
2
NADAL ET AL
Fig 1. Fibrous crescent with disruption of Bowman’s capsule, glomerular tuft collapse, and segmental sclerosis (PAS, original magnification ⴛ200).
The arterioles and small and medium-sized arteries were normal. Fluorescence microscopy disclosed 2 to 3⫹ segmental to global coarse granular deposits in isolated glomerular capillary walls and also mesangium of immunoglobulin (Ig) M, C1q, and C3, whereas IgG, IgA, and fibrinogen were negative. The deposits in the capillary wall and mesangial matrix were Congo red negative and thioflavine-T negative. Electron microscopy of nonsclerosed glomeruli showed mesangial expansion and widening of the basement membranes of glomerular capillaries. Granular and fibrillary nonbranching deposits were observed in subendothelial and mesangial areas. The fibrils were randomly arranged and had a diameter slightly larger than amyloid fibrils (Fig 2). The final histological diagnosis was fibrillary glomerulonephritis. The patient continued with restrictions of salt and protein in his diet, and his blood pressure was normalized, changing enalapril for nifedipine. In December 1995, he showed uremic syndrome with blood urea of 88.5 mmol/L (248 mg/dL); creatinine, 778 µmol/L (8.8 mg/dL); and endogenous creatinine clearance of 8.8 mL/min, and he started hemodialysis.
More than 12 patients have been reported in the literature with the association of CMT and glomerulopathies. Moreover, Gherardi et al3 and Denian et al6 concluded that focal segmental glomerulosclerosis was the morphological lesion found in all reported patients with CMT. However, a case of immune complex glomerulonephritis in a patient with CMT also has been described.7 In addition, Paul et al8 described two patients (mother and daughter) who had CMT associated with renal involvement. The child was studied with renal biopsy and showed, in electron microscopy, thinning and splitting of the basement membrane as in Alport disease. No fibrillary deposits were found. Renal biopsy was not performed on the mother. The pattern and distribution of the deposits in immunofluorescence microscopy in our patient suggest the possibility of IgM, C1q, and C3 trapping in the widened mesangium, sparce capillary walls, and sclerotic areas. These findings seem to be similar to other, previously reported cases of CMT associated with focal and segmental glomerulosclerosis.8
DISCUSSION
In this patient, the diagnosis of hereditary peripheral neuropathy of CMT type 1 was made on the basis of the insidious onset of distal muscle weakness and wasting in the lower limbs, areflexia at the ankles, evidence of demyelinating neuropathy on motor nerve conduction studies, and duplication of chromosome 17, which encodes the peripheral myelin protein 22 gene.4 CMT is usually transmited by autosomal dominant inheritance, but an autosomal recessive pattern also has been described. The absence of neurological disorders in our patient’s parents is more compatible with a recessive autosomic variant.5
Fig 2. Electron micrograph shows randomly arranged microfibrils in the subendothelial space of the glomerular capillary (Original magnification ⴛ30,000).
FIBRILLARY AND CHARCOT-MARIE-TOOTH DISEASE
3
Conversely, deposits of IgG and C3 have been found in many cases of FG. However, they were scant or negative in our patients, as they were in some of the reported cases with FG. This might be attributed to the advanced sclerosing stage present in this biopsy specimen. Electron microscopy of renal tissue was performed in five of these cases with CMT, and no fibrillary deposits were shown.3,6,8-10 However, we cannot exclude some other case of FG among those patients who were not studied by electron microscopy. FG is an unusual primary kidney disease,11 characterized by deposition of immunoglobulins in a fibrillar pattern that resembles amyloid but does not stain with Congo red. In a report of a series of patients with this glomerulopathy, Duffy et al12 used the term fibrillary to describe the characteristic ultrastructure of the immune deposits. After this, Alpers et al13 proposed the name FG for this disease. The case described in our report had the typical clinical manifestations of FG, such as heavy proteinuria, arterial hypertension, and progressive renal insufficiency, and it lacked evidence of systemic lupus erythematosus, cryoglobulinemia, amyloidosis, or light chain deposition disease. The patients’ age at discovery of FG is frequently between 40 and 50 years, but typical cases have been reported in patients from 10 to 80 years of age,14 as in our young patient. On electron microscopy, the renal biopsy specimen showed the fibrillar deposits that were randomly oriented and located in the mesangial matrix and the endothelial side of the glomerular basement membrane. This finding has been essential for the diagnosis of FG. FG is pathologically characterized by fibrillar deposits that can be 10 to 30 nm in diameter. There is a debate about whether FG differs from the so-called immunotactoid glomerulopathy, in which microtubular structures ranging from 18 to 90 nm in diameter are seen. The question must await further study.15,16 Although recent reviews of FG have emphasized a lack of extrarenal manifestations, some data suggest that these patients infrequently can show involvement in other organs.17,18
Furthermore, the association of FG with other conditions has been reported.19-24 Because FG is an entity of uncertain origin and pathogenesis, and CMT is a genetic abnormality, we think that the juxtaposition of both diseases could be considered merely fortituous. This case of FG is remarkable because we have not found any prior description of its association with CMT in the literature. REFERENCES 1. Rosenmann E, Eliakim M: Nephrotic syndrome associated with amyloid-like glomerular deposits. Nephron 18:301308, 1997 2. Panner BJ: Rapidly progressive glomerulonephritis and possible amyloidosis. Arch Pathol Lab Med 104:603609, 1980 3. Gherardi R, Beighti-Deprez D, Hirbec G, Bouche P, Weil B, Lagrue G: Focal glomerulosclerosis associated with Charcot-Marie-Tooth disease. Nephron 40:357-361, 1985 4. Lebo RV, Martelli L, Su Y, Li L, Lynch E, Mansfield E, Pua KH, Watson DF, Chue J, Hurko O: Prenatal diagnosis of Charcot-Marie-Tooth disease type 1A by multicolor in situ hybridization. Am J Med Genet 47:441-450, 1993 5. Ionasescu V, Zellweger H: Genetics in neurology, pp 374-392. New York, NY, Raven Press, 1983 6. Deniau F, Guillot M, Plus A, et al: Maladie de CharcotMarie-Tooth et ne´phropatie glomerulaire. Arch Fr Pediatr 43:791-793, 1986 7. Yudis M, Sirota RA: Immune complex glomerulonephritis in Charcot-Marie-Tooth disease. Am Soc Nephrol p 48A, 1982 (abstr) 8. Paul MD, Fernandez D, Pryse-Phillis W, et al: CharcotMarie-Tooth disease and nephropathy in a mother and daughter with a review of the literature. Nephron 54:80-85, 1990 9. Hara M, Ichida F, Higuchi A, et al: Nephropathy associated with Charcot-Marie-Tooth disease. Int J Pediatr Nephrol 5:99-102, 1984 10. Lloveras JJ: Focal glomerulosclerosis and CharcotMarie-Tooth disease, not a chance association? Nephron 43:231, 1986 11. Iskandar SS, Falk RJ, Charles Jennette J: Clinical and pathologic features of fibrillary glomerulonephritis. Kidney Int 42:1401-1407, 1992 12. Duffy L, Khurana E, Susin M, et al: Fibrillary renal deposits and nephritis. Am J Pathol 113:279-290, 1983 13. Alpers CE, Rennke HG, Hooper J Jr, et al: Fibrillary glomerulonephritis: An entity with unusual immunofluorescence features. Kidney Int 31:781-789, 1997 14. Korbet SM, Schwartz M: Immunotactoic glomerulopathy. Am J Kidney Dis 17:247-257, 1991 15. Alpers CE: Fibrillary glomerulonephritis and immunotactoid glomerulopathy: Two entities, not one. Am J Kidney Dis 22:448-451, 1993 16. Schwartz MM: Immunotactoid glomerulopathy: The case for Occam’s Razor. Am J Kidney Dis 22:446-447, 1993 17. Masson RG, Rennke HG, Gottieb MN: Pulmonary hemorrage in a patient with fibrillary glomerulonephritis. N Engl J Med 326:36-39, 1992
4
18. Ozawa K, Yamabe H, Fukushi K, et al: Case report of amyloid-like glomerulopathy with hepatic involvement. Nephron 58:347-350, 1991 19. Kohan DE, Perkins SL, Terreros DA: Immune complex glomerulonephritis with unusual microfibrilar deposits associated with primary bone marrow lymphoma. Am J Kidney Dis 21:47-51, 1993 20. Orfila C, Meeus F, Bernadet P, et al: Immunotactoid glomerulopathy and cutaneous vasculitis. Am J Nephrol 11:67-72, 1991 21. Schifferli JA, Merot Y, Cruchaud A, et al: Immunotactoid glomerulopathy with leucocytoclastic skin vasculitis
NADAL ET AL
and hypocomplementemia: A case report. Clin Nephrol 27:151-155, 1987 22. Rosenmann E, Brisson ML, Bercovitch DD, et al: Atypical membranous glomerulonephritis with fibrillar subepithelial deposits in a patient with malignant lymphoma. Nephron 48:226-230, 1988 23. Abraham G, Bargam JM, Blake PG, et al: Fibrillary glomerulonephritis in a patient with metastatic carcinoma of the liver. Am J Nephrol 10:251-254, 1990 24. Alonso R, Novoa D, Alonso MC, et al: Nonamyloidotic fibrillar glomerulopathy and rheumatoid arthritis. Nephron 63:120-121, 1993