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A 50s man receiving dialysis for chronic kidney disease due to IgA nephropathy underwent laparoscopic reversal via Hartmann 's procedure for rectal cancer and multiple liver metastases, followed by chemotherapy for the liver metastases. Following a single course of mFOLFOX therapy, bevacizumab was administered for 8 courses, resulting in tumor shrinkage and a decrease in tumor marker levels. The initial doses were 60mg/m2 oxaliplatin and 280(bolus injection)and 1,680mg/m2 (continuous infusion)of 5-FU. Subsequently, these doses were adjusted to be administered every 3 weeks. No serious adverse events other than neutropenia(Grade3 ), anorexia(Grade1 ), and hiccups(Grade1)were noted.

We report a 40-year-old man with end-stage renal disease due to IgA nephropathy who underwent deceased donor kidney transplantation. The donor was diagnosed to be brain-dead due to cerebral hemorrhage after her second liver transplantation for non-viral liver cirrhosis. Intraoperative 1-hour biopsy of the graft kidney revealed moderate global glomerular sclerosis (22%) and interstitial fibrosis (40%) consistent with underlying nephrosclerosis or calcineurin inhibitor nephrotoxicity. Although hemodialysis was needed until the graft began functioning several days after the kidney transplantation, the postoperative clinical course thereafter was uneventful and the graft functioned well with stable serum creatinine levels around 2.4 mg/dl at 6 monthspos toperatively.

We report a case of testicular malignant lymphoma in a hemodialysis patient. A 65-year-old man who had been undergoing hemodialysis for 8 years and 10 months consulted our hospital with right testicular enlargement in August 2012. Under a diagnosis of testicular cancer from manipulation test and ultrasonography, high orchiectomy was performed. Computed tomography showed swelling of the retroperitoneal lymph nodes. Histopathological examination revealed diffuse, non-Hodgkin B-cell lymphoma, CD20＋. R-CHOP chemotherapy was initiated and retroperitoneal lymph node swelling completely disappeared after 1 cycle of chemotherapy. After completing 2 cycles of chemotherapy, the patient developed interstitial pneumonia, and thus radiotherapy to the retroperitoneal space including the left testis was performed. As of July 2014, the patient remains alive without recurrence.

We report herein on a patient with unexpected trismus after the induction of general anesthesia due to temporomandibular arthrosis. A 30 year old man visited our hospital complaining of hematuria, and he was scheduled for bil tonsillectomy under general anesthesia. Preoperative examination revealed no evidence of difficult airway and no sign of trismus. Despite the administration of muscle relaxants, it was impossible to expand the operative field due to by trismus after the introduction of general anesthesia. Malignant hyperthermia was excluded, and the trismus was judged to be due to temporomandibular arthrosis. Manual repositioning was performed, trismus was improved and expansion of the surgical field became possible. During any head and neck surgical procedure, if an otolaryngologist should encounter trismus after the induction of general anesthesia, temporomandibular arthrosis should be borne in mind if temporomandibular arthrosis is diagnosed as the cause, manual repositioning should be employed as soon as possible.

Bevacizumab, an inhibitor of vascular endothelial growth factor, is approved for the treatment of various cancers, but the incidence of proteinuria as a side effect has been reported to be 2-64%. We report a case of renal impairment due to thrombotic microangiopathy (TMA) accompanied with glomerular subendothelial deposition of IgA resulting from bevacizumab administration. A 57-year-old female with advanced breast cancer, to whom bevacizumab had been administered from October 2012, developed proteinuria and epithelial casts in her urine about a month later. Serum creatinine remained at 0.7-0.8 mg/dL until June 2013, but gradually increased to 1.3 mg/dL in September. She was referred to our hospital because her renal function had not improved despite termination of bevacizumab, and a renal biopsy was performed in October. At that time, the levels of proteinuria, serum creatinine and serum IgA were high at 1.3 g/g x Cr, 1.6 mg/dL and 430 mg/dL, respectively. Histological examinations showed prominent IgA deposits in the subendothelial area and glomerular infiltration of CD68 positive cells in addition to features of TMA, such as narrowed glomerular capillary lumina and double contours of the basement membranes. In consideration of her clinical history, a diagnosis of bevacizumab-induced TMA was made. Through follow-up care without readministration of bevacizumab, epithelial casts in her urine disappeared, and proteinuria decreased to 0.62 g/g x Cr in November. Serum creatinine remains high at around 1.3 mg/dL, but has not elevated further. Serum IgA gradually decreased and reached 289 mg/dL in April 2014. TMA due to bevacizumab described in several other reports was also accompanied by glomerular IgA deposition, thus a differential diagnosis of IgA nephropathy is required. TMA was recently added to a section of "significant adverse effects" in the package insert of bevacizumab. Nephrologists should be fully aware of this drug-induced nephropathy.

A 34-year-old woman with underlying IgA nephropathy was admitted to our hospital with chief complaints of abdominal pain and pyrexia. Computed tomography showed increased mural thickness of the ileum and increased mesenteric fat density. Colonoscopic findings revealed a longitudinal ulcer in the terminal ileum and irregularly shaped ulcers and a longitudinal ulcer scar in the descending colon. Histopathological analysis of biopsy specimens from the ileum and descending colon showed non-caseating epithelioid cell granuloma. On the basis of these findings, the condition of the patient was diagnosed as ileocolonic Crohn's disease, and the patient received parenteral nutrition, followed by elemental diet. The patient was responsive to nutrition therapy, and the amount of uric protein decreased as her Crohn's disease activity index decreased. In conclusion, we assume that the Crohn's disease activity correlated with that of IgA nephropathy.

Objective: Pregnancy in chronic kidney disease (CKD) patients is often associated with hypertension and/or the worsening of renal function and neonatal death. The present study explored the clinical characteristics of predictive factors for hypertension in biopsy-proven IgA nephropathy patients with superimposed preeclampsia (SPE)., Patients and Methods: The subjects were 34 Japanese women with IgA nephropathy whose renal specimen for histological tests was obtained before pregnancy. We retrospectively investigated the relevant clinical factors to explain a rise in blood pressure (BP). The histological findings were evaluated with respect to the quantitative measurements of both global glomerulosclerosis and interstitial damage., Results: Renal biopsies before pregnancies showed that the global glomerular sclerosing index and interstitial damage in the SPE group were significantly higher than in the normal group. The prevalence of SPE was 38.2 % (normal pregnancy 21, SPE 13 cases). The neonatal death rate was 3.0 % (1/34)overall. Just before conception, systolic blood pressure (SBP), serum creatinine (Cr)and blood urea nitrogen (BUN) concentration in the SPE were significantly higher than in normal pregnancies. In contrast, CCr and eGFR were lower in the SPE group than in the normal group. At delivery, serum Cr, BUN and uric acid (UA) concentration in the SPE group were significantly higher than in the normal group. In contrast, CCr and eGFR were lower in the SPE than in the normal group. At delivery, correlation analysis revealed a significant correlation between SBP or diastolic BP (DBP) and the histological severity, between SBP or DBP and daily protein excretion, and between SBP or DBP and serum Cr concentration. With respect to the birth weight of newborns, there was a significant negative correlation between the birth weight and the global glomerular sclerosing rate, and between the birth weight and serum Cr concentration or BUN. A stepwise multiple regression analysis showed that predictive factors for a rise in SBP during pregnancy were the degree of interstitial damage and daily urinary protein excretion. These results suggest that renal function, the magnitude of urinary protein excretion, serum Cr, BUN, UA concentrations, and the severity of histological abnormalities are all associated with SPE occurrence. The predictors of a rise in BP were interstitial damage and urinary protein excretion at pregnancy. In addition, Receiver Operating Characteristic (ROC) analysis showed that both glomerular sclerosis and interstitial damage could be potential predictors for SPE., Conclusion: Histological severity in renal biopsy, urinary protein excretion and renal function are associated with SPE in patients with IgA nephropathy. Among these associations, the histological findings and urinary protein excretion may serve as useful predictors for a rise in BP.

We report a case of IgA nephropathy with tuberculous pleurisy that was treated with steroid pulse therapy combined with tonsillectomy. A 27-year-old female was referred to our hospital because of hematuria and proteinuria. Her urinalysis showed mild proteinuria (0.7 to 0.9 g/day) with dysmorphic red blood cells and cellular casts. Her serum creatinine level was within the normal range. Renal biopsy specimens revealed mild mesangial proliferation with cellular crescent and adhesion of glomeruli to the Bowman's capsule. Tubulointerstitial changes including mononuclear cell infiltration and tubular atrophy were also observed. Immunohistochemical staining of IgA and C3 was detected in the mesangial area, leading to the diagnosis of IgA nephropathy. She had a past history of tuberculous pleurisy at 13 years of age and had taken antituberculosis drug for one and a half year. Although treatment with angiotensin receptor antagonist was started, the amount of proteinuria was not changed. Steroid pulse therapy with tonsillectomy followed by oral prednisolone 20 mg/day was conducted. Proteinuria and hematuria gradually decreased. Her respiratory status and chest X-ray had been closely followed up by her respiratory physician. After one and a half years of treatment with low-dose prednisolone, her urinalysis became almost normal. Recurrence of tuberculosis was not observed during the follow-up period. The successful outcome of this case encouraged us to treat IgA nephropathy with a past history of tuberculosis using interventions including steroid pulse therapy.

A 60-year-old man, who had been diagnosed as having paroxysmal nocturnal hemoglobinuria(PNH) in 1994, was admitted to our hospital with general fatigue, and dark urine after a common-cold in January 2001. In the peripheral blood, the red blood cell count was 136 x 10(4)/microl, hemoglobin 4.0 g/dl and hematocrit 12.4%. The serum creatinine level was 9.9 mg/dl. Kidney biopsy revealed focal and segmental proliferation of mesangial cells, mesangial matrix expansion, acute tubular necrosis, interstitial fibrosis and hemosiderine deposits in the tubular epithelial cells confirmed by Berlin-blue staining. Immunofluorescence microscopy showed IgA and C3 deposition in the mesangium. Electron microscopy revealed electron dense deposits in the mesangial area and heavy electron-dense hemosiderin pigments in proximal tubular epithelial cells. After the transfusion of six units of washed red blood cells and two sessions of hemodialysis, the renal function returned to the levels before admission.

The recipient, a 31-year-old man, was diagnosed with severe diffuse hypokinesis of left ventricle and diastolic dysfunction by echocardiography before the renal transplantation. His left ventricular ejection fraction (LVEF) was 29%. Therefore we had to postpone the operation and tried to improve his cardiac function. We controlled his dry weight more strictly with hemodialysis and limited in take of salt and water to reduce preload of his heart and administered erythropoietin to improve his anemic condition. We administered angiotensin-converting enzyme inhibitors (ACEI) to control his blood pressure and reduce afterload of his heart. Two months later, his cardiac function was marked improved (LVEF, 29% to 47%), and he underwent renal transplantation. Five months after the operation, improvement of his cardiac function kept on being observed in spite of the cessation of treatment for his heart (LVEF, 47% to 68%). Successful renal transplantation can significantly improve the cardiac function of patients on maintenance dialysis.

A 24-year-old Japanese woman with IgA nephropathy was admitted to our hospital due to the development of proteinuria and pretibial edema while on glucocorticoids and an angiotensin-converting-enzyme(ACE) inhibitor. She had been on both medications for more than 2 years. Urinary protein excretion was 2.53 g/day and renal function laboratory data were within the normal range. Plasma aldosterone concentration was high at 248 pg/ml, with normal plasma renin activity. The renal biopsy specimens showed prominent glomerular hypertrophy. Four weeks after the addition of valsartan, an angiotensin II receptor blocker(ARB), urinary protein excretion was remarkably reduced to 0.6 g/day without adversely affecting blood pressure. During the treatment period, proteinuria was maintained at less than 0.6 g/day and renal function remained normal. We propose that glomerular hypertension caused by insufficient suppression of the renin-angiotensin system was an essential factor underlying the increased urinary protein excretion in this patient. Combination therapy of an ARB and an ACE inhibitor appears to have a beneficial effect in patients with IgA nephropathy patients with persistent glomerular hypertension.

A 74-year-old man who had undergone artificial pneumothorax therapy for pulmonary tuberculosis 40 years earlier was admitted because of blurred vision, headache, and numbness of the lower limbs in October 1997. He presented with anemia and leukocytopenia with monoclonal gammopathy of IgM (kappa). His bone marrow was diffusely infiltrated with small lymphocytes, plasmacytoid lymphocytes, and plasma cells expressing IgM, kappa surface immunoglobulin. On the basis of these findings, primary macroglobulinemia (PMG) was diagnosed. CT scan of the chest demonstrated pleural effusion of the right lung encapsulated in a thickened pleura, and pseudochylothorax was diagnosed from a specimen of chyliform fluid which contained numerous cholesterol crystals and was positive for Mycobacterium tuberculosis (MT) on PCR assay. The patient's condition was also complicated by chronic renal failure due to IgA nephropathy, which may have been a consequence of the tuberculosis, possibly due to an abnormal IgA-mediated immune response to MT. The patient gradually developed pure red cell aplasia during the course, probably due to an autoimmune mechanism. Later in the course, immunoglobulin gene analysis of the malignant cells of PMG showed that they were derived from antigenically selected cells. In the context of antigenic stimulation, the role of MT antigen in the pathogenesis of PMG was of interest in this patient.

A 72-year-old man was admitted for examination of dyspnea and pitting edema of the lower legs in July, 1996. His hemoglobin level was 6.9 g/dl, and myelodysplastic syndrome (MDS) was revealed by bone marrow aspiration, and frequent transfusions were needed. His renal function rapidly deteriorated in the middle of August (BUN 45 mg/dl, Cr 4.8 mg/dl) and IgA nephropathy (IgAN) with marked intestinal nephritis was disclosed by renal biopsy. In November, joint manifestations of warmth and pain, which suggested arthritis, appeared at the bilateral wrist and ankle joints. Soon after receiving prednisolone (20 mg/day), the arthritis was relieved. Renal function also improved (BUN 41 mg/dl, Cr 21 mg/dl) and frequent transfusions were no longer necessary. This is a case with various clinical manifestations of MDS, IgAN, and arthritis, and appears to be the first MDS case complicated with IgAN. A number of case reports have identified immune abnormalities in patients with MDS. Immune and bone marrow abnormalities have been reported to be involved in the pathogenesis of IgAN. Thus, MDS could be complicated by IgAN. Their pathogenetic association is discussed in this paper.

We report a case of a 37-year-old man with relapsing polychondritis and IgA nephropathy. He visited our hospital with high fever and the swelling of his ears and eyelids. His symptoms and the results of the biopsy of his right auricle fulfilled the Damiani's criteria. Laboratory examination on admission showed an increase of serum IgA level, a presence of immune complex, remarkable hematuria (grade III) and proteinuria (grade II). Most of his symptoms were improved by the administration of antibiotic and NSAIDs, however, urinary findings still remained unchanged. The biopsy of his right kidney led to a diagnosis of IgA nephropathy (group II). Although relapsing polychondritis is known to associate rarely with renal involvement, it is very rare to associate with IgA nephropathy. This case indicates that immune disorders including IgA nephropathy should be investigated in patients with relapsing polychondritis.

We have encountered a 49-year-old female with persistent proteinuria and hematuria. Blood pressure, renal function, physical findings and chest X-p showed no abnormality, but blood tests disclosed mild thrombocytopenia, elevated serum ACE activity, serum lysozyme activity and serum IgA concentration. Abdominal echography and CT revealed multiple nodules in her spleen. In order to make a definite diagnosis and exclude the possibilities of malignant lymphoma or metastatic malignant tumor, splenectomy, and open renal biopsy were performed at the same time. On histological examinations, light microscopic appearance of the spleen was characterized by non-caseating granulomas compatible with sarcoidosis. Renal biopsy specimen showed diffuse proliferative glomerulonephritis with positive staining of IgA predominantly located in the mesangial area, compatible with IgA nephropathy. The present case may provide suggestive evidence for a link between sarcoidosis and IgA nephropathy in the pathogenesis. IgA nephropathy complicated by sarcoidosis is rare, and thus is of particular interest because common immunological abnormalities might be considered in the disease process of both diseases. We feel that despite a low index of suspicion, physicians must be alert to the possibility of IgA nephritis associated with sarcoidosis. The literature is reviewed regarding the relationship between IgA nephropathy and sarcoidosis.

Using 100 serial sections for light microscopy, we studied the clinicopathologic characteristics of IgA nephropathy with severe proteinuria. Eight out of 128 cases with IgA nephropathy exhibited severe proteinuria of 3.0g/day or more. These cases consisted of 5 males and 3 females with an age range from 15 to 73 years. Daily proteinuria ranged from 3.3 to 7.1 g. At the time of biopsy, the serum creatinine level was 1.2 mg/dl or more in 6 cases; two of these developed end-stage renal failure during the follow-up period. In most of the cases, routine sections for light microscopy revealed moderate to severe mesangial proliferation and tubulointerstitial damage. In 7 cases, variable percentages of glomeruli, ranging from 20% to 95%, were involved by chronic lesion represented by sclerosis and fibrous crescents/adhesion, while only 2 cases exhibited active lesion characterized by segmental glomerular necrosis and/or cellular/fibrocellular crescents. In contrast, thorough observation of 100 additional serial sections disclosed the focal presence of active lesion in all except one case with features of endstage kidney. In addition, the highest percentage of glomeruli with active lesion in the serial sections correlated well with the severity of proteinuria. The results suggested that severe proteinuria in IgA nephropathy depends on, at least in part, focal outbreak of active lesion characterized by segmental glomerular necrosis and cellular/fibrocellular crescents.

A 73-year old man was admitted to the hospital because of dyspnea. His proteinuria was pointed out in 1981. He felt dyspnea after exertion and abnormal chest X-ray shadow was pointed out in 1984. He was admitted to our hospital for further examination for the first time in 1988. He was diagnosed as IgA nephropathy by renal biopsy, and idiopathic interstitial pneumonia (IIP) by transbronchial lung biopsy. Then steroid therapy was begun because of progression of renal dysfunction in November 1990. But thereafter dyspnea, hypoxia and fine diffuse reticulonodular shadow on chest X-ray film was exacerbated. And he died because of respiratory failure. In this case, progression of IgA nephropathy seemed associated with exacerbation of IIP.

In order to examine further the role of the electrical change of IgA in the pathogenesis of IgAN, we studied the charge distribution of serum IgA in IgAN with episodes of macrohematuria. Blood samples were taken from 20 IgAN patients during bouts of macrohematuria and again more than 3 months later. Twenty healthy adults were used as controls. All samples were focused by Multiphor II flatbet electrofocusing unit apparatus (LKB) on an agarose gel (0.8% isogel agarose-EF, 2.5% pharmalyte 4.0-6.5). The focused gels were incubated with polyclonal goat anti-human IgA and were washed in several changes of saline for 48 hours. Immunofixed materials remaining in the gels after washing were fixed and stained with coomassie brilliant blue R250. The stained gels were analysed by densitometry. The relative areas of the individual peaks and their proportional contributions to the total IgA spectrotype were determined by computer. The results were as follows: 1. The percentage of proportional contribution of IgA peaks (pI 4.7-5.15) in IgAN were higher in patients than in controls (p less than 0.01). 2. The percentage of proportional contribution of IgA peaks (pI 4.9-5.05) in IgAN at bouts of macrohematuria was higher than in the same patients when not undergoing episodes of macrohematuria (p less than 0.01). These results suggest that the excess amount of anionic IgA may contribute to the pathogenesis of IgAN.

We performed enucleation on a patient with renal cell carcinoma associated with nephritis to preserve renal function. The patient was a 40-year-old man diagnosed with chronic nephritis. Ultrasonography performed during brief hospitalization for a check-up revealed a tumor in the left kidney. Enucleation was performed to treat stage 1 renal cell carcinoma. Pathological study revealed that the patient had IgA nephropathy and grade 1 clear cell carcinoma.

We performed 308 series renal biopsies during 4 years (1985-1989) and 289 cases were examined by light microscopic, electron microscopic, or immunofluorescent study. Clinically, chronic nephritic syndrome was most frequent (55.4%), followed by nephrotic syndrome (15.1%), and recurrent or persistent hematuria (12.8%). Pathologically, IgA nephropathy was most popular (39.3%), followed by normal glomerulus (9.1%), and thin basement membrane disease (8.7%). Glomerulonephritis clinically recognized with recurrent or persistent hematuria, hardly showing proteinuria, in 81.6% of the cases, consisted of normal glomerulus, or thin basement membrane disease by electron microscopic and immunofluorescent examinations. The remainder (18.4%) was with IgA nephropathy, which was histologically mild. On the other hand, cases of chronic nephritic syndrome (latent type) with persistent proteinuria and hematuria were with glomerulonephritis of various types including IgA nephropathy in 78.8% of the total cases. Therefore, proteinuria is an important sign of glomerulonephritis. In investigation in different age groups, IgA nephropathy was seen in about 40% of both pediatric and adult cases, whereas minor glomerular abnormalities and thin basement membrane disease were more frequent in pediatric cases. Tubulo-interstitial lesions and glomerular lesions in vascular or metabolic diseases were recognized more in adults than in children. Membranous glomerulonephritis (17 cases including 4 pediatric cases), complicated with malignant tumors such as bladder or rectal cancers and hepatoma was found in 3 aged patients. Examination for malignant tumor would be necessary for aged patients with membranous glomerulonephritis. As for the prognosis of IgA nephropathy, because histological changes of IgA nephropathy varied widely from very mild state to severe state, the prognosis is not always good.(ABSTRACT TRUNCATED AT 250 WORDS)

A 34-year-old man was admitted to Prier hospital because of head and right foot injuries caused by a traffic accident. Two months after admission, he complained of abdominal pain and bloody stool. Shortly after purpura appeared on both legs. He received an exploratory laparotomy and showed multiple jejunal ulcer. A pathological examination of the jejunum revealed necrotizing vasculitis of the small arteries. After the operation, he had arthralgia and the laboratory examination showed massive urinary protein. Arthralgia, abdominal pain and bloody stool disappeared with the administration of 100 mg per day of prednisolone (PSL), but nephrotic syndrome was not relieved. As a result he was referred to our hospital. And after admission, PSL was gradually tapered to 60 mg per day. Then an open renal biopsy was performed, and pathological examinations revealed focal proliferative glomerulonephritis in which 31% of the glomerulus showed fibro-cellular crescents. A direct immunofluorescence of the renal biopsy showed mesangial deposits of IgA, IgG, C3. The patient was treated with anti-coagulant therapy and PSL. Urinary protein was gradually decreased to 0.7 g/day, and his creatinine clearance was 23 ml/min five months after the renal biopsy. In this case, although the renal biopsy specimens and clinical symptoms were compatible with HSP, a pathological examination of jejunum revealed vasculitis of the small arteries. In literature, HSP is a syndrome characterized by vasculitis of arterioles, capillaries and venules. As a results of those findings, we think the diagnosis of this patient is PN with mesangial IgA depositions of renal glomeruli.

Urinary protein fractions and clinicopathological features in 80 patients with IgA nephropathy, who had mild proteinuria (0.60 +/- 0.35 g/day) less than 2 g/day, were analyzed. Urinary protein fractions was determined with SDS-polyacrylamide microgel electrophoresis (SDS-PAGE). The patterns on the densitogram of SDS-PAGE were divided into 4 groups, that is, normal pattern (Group I: N = 4), low molecular weight proteins (LMWP) predominant pattern (Group III: N = 29) and high molecular weight proteins (HMWP) excessive pattern (Group IV: N = 28). Histological changes were minor in majority of Group I but gradually increased in Group II, III and IV. Especially in Group IV, global sclerosis (78.6%; vs. Group II: p less than 0.01, vs. Group III: p less than 0.05), small crescent (57.1%; vs. Group II: p less than 0.05), adhesion (60.7%; vs. Group II: p less than 0.05), mesangial proliferation (96.4%; vs. Group II: p less than 0.01, vs. Group III: p less than 0.05) and tubulointerstitial degeneration (85.7%; vs. Group II and III: p less than 0.05) were most predominant. These results indicate that urinary protein fractions and histological changes appear to correlate closely in IgA nephropathy with mild proteinuria, and that marked HMWP is considered to be an early marker of glomerular damage in the prognosis of IgA nephropathy.

A 52-year-old man, who had been diagnosed as having alcoholic liver cirrhosis, presented a chronic nephritic syndrome due to hepatic glomerulosclerosis. Ten months before death, massive proteinuria exceeding 40 g/day was noted. A renal biopsy revealed diffuse mesangial sclerosis, associated with an IgA deposition consistent with hepatic glomerulosclerosis. Although the nephrotic syndrome subsided with immunosuppressive therapy, he died of hepatic failure. Postmortem examinations disclosed a diffuse, medium-size B-cell lymphoma, involving the peritoneal and retroperitoneal organs and an IgA-positive plasmacytosis. His massive proteinuria seems to have been caused by the paraneoplastic syndrome of a malignant lymphoma.