A case of Lemierre syndrome combined with a suspected systemic lupus erythematosus flare.

Lemierre syndrome develops in healthy young patients as a result of bacteremia after oral cavity infection. It causes thrombophlebitis in the internal jugular vein. Infection can easily occur during immunosuppressive treatment in patients with systemic lupus erythematosus and become severe. We present a case of Lemierre syndrome in a patient with systemic lupus erythematosus. A 56-year-old woman presented with fever, left lower toothache, and skin symptoms from the left neck to the anterior chest. Clinical presentation and laboratory investigations revealed Lemierre syndrome. The inflammation and thrombus disappeared with antibiotic and anticoagulant therapies. However, transient hypocomplementemia and elevated antinuclear antibody levels were observed during treatment; therefore, a concomitant systemic lupus erythematosus flare was considered. In systemic lupus erythematosus patients with Lemierre syndrome, complement and antinuclear antibody levels are modified, so other indicators should be precisely evaluated, such as levels of urinary protein, sediment, serum creatinine and anti-dsDNA antibody, and systemic lupus erythematosus disease activity index.

Nephrotic syndrome associated with ramucirumab therapy: A single-center case series and literature review.

Ramucirumab is a human immunoglobulin G1 monoclonal antibody that binds to vascular endothelial growth factor receptor 2 and is used for the treatment of metastatic or inoperable gastric, colorectal, and non-small cell lung cancers. However, ramucirumab can result in renal adverse events, including nephrotic syndrome, and the clinical course of this event is unclear. This study aimed to investigate the clinical course and pathological findings of patients with nephrotic syndrome after ramucirumab treatment.We evaluated 5 patients with malignancies (2 cases of gastric cancer and 3 cases of colorectal cancer) who developed nephrotic syndrome during treatment with ramucirumab. Two patients were diagnosed based on renal biopsy. We investigated the relationship between ramucirumab treatment and clinical courses, pathological findings, and renal outcomes.Four of 5 patients developed nephrotic syndrome after 1 or 2 doses of ramucirumab. All patients had hypertension, and 2 of 5 patients had renal dysfunction, defined as an increase in serum creatinine levels of ≥50% or ≥0.3 mg/dL. The 2 renal biopsy samples revealed a diffuse glomerular basement membrane double contour, intracapillary foam cell infiltration, and partial foot process effacement. Early drug discontinuation and antihypertensive therapy improved proteinuria, renal dysfunction, and hypertension in all patients.Nephrotic syndrome is a renal adverse event observed in cancer patients after ramucirumab treatment. We suggest that urinalysis, renal function, and blood pressure should be closely monitored in patients undergoing ramucirumab treatment, and treatment should be discontinued if renal adverse events are detected.

A case of entecavir-induced Fanconi syndrome.

Acquired Fanconi syndrome has been associated with the long-term ingestion of several nucleoside analogs used to treat chronic hepatitis B virus infection. However, the nucleoside analog entecavir has not been found to cause nephrotoxicity. We report a case of entecavir-induced Fanconi syndrome. Our patient was a 73-year-old man admitted to our hospital because of renal dysfunction. He also presented with hyperaminoaciduria, renal diabetes, phosphaturia, hypophosphatemia, hypokalemia, hypouricemia, and hyperchloremic metabolic acidosis, supporting a diagnosis of Fanconi syndrome. In this case, the cause of Fanconi syndrome was most likely entecavir, which had been administered as needed depending on his renal function for 5 years. After drug discontinuation and replacement with tenofovir alafenamide fumarate therapy once a week, the patient's kidney function recovered and electrolyte anomalies partially improved. We highlight the fact that entecavir may induce severe renal dysfunction, which can cause the development of Fanconi syndrome; therefore, close monitoring of proximal tubular function is recommended during entecavir therapy.

A suspected case of drug-induced tubulointerstitial nephritis by pilocarpine hydrochloride.

A 63-year-old man with pharyngeal cancer had been prescribed pilocarpine hydrochloride for xerostomia after concomitant chemoradiotherapy. After 6 months of taking pilocarpine hydrochloride, he was referred to our hospital due to gradually developing renal insufficiency. The patient underwent detailed urinalysis, blood chemistry analysis, immune-serology testing. A renal biopsy was also performed. He was diagnosed with chronic tubulointerstitial nephritis (TIN) caused by lymphocytic infiltration of the interstitium, tubular atrophy, and interstitial fibrotic changes. Infections, autoimmune diseases, and genetic factors were ruled out as causes of TIN; a drug-induced lymphocyte stimulation test confirmed that he had high stimulation index scores for pilocarpine hydrochloride and a normal range stimulation score for other supplements. These results indicated that the TIN could have been induced by pilocarpine hydrochloride. Drug discontinuation partly improved his renal function and tubule marker levels. To our knowledge, this is the first report of TIN following administration of pilocarpine hydrochloride. This finding could contribute to future treatment decisions for patients with TIN and those using pilocarpine hydrochloride.

Hematuria Alone or in Combination with Proteinuria Is a Harbinger of Poor Prognosis in Patients with Non-Hodgkin Lymphoma.

BACKGROUND: Screening for hematuria is essential during health checkups in the general population. However, urine examinations in patients with cancer tend to be overlooked. This study attempted to demonstrate the novel utility of urinalysis in the assessment of the prognosis of non-Hodgkin lymphoma (NHL). METHODS: A longitudinal, retrospective cohort study was conducted to examine the association between hematuria and mortality in 294 patients with NHL. Urinalysis was performed using a dipstick test. A multivariate, logistic regression model was constructed to evaluate factors associated with the presence of hematuria. Statistical association between hematuria and the time to all-cause mortality was analyzed using Kaplan-Meier analysis, followed by multivariate proportional hazards regression analysis adjusted for covariates that might be related to mortality. RESULTS: The prevalence of hematuria alone and in combination with proteinuria was 11.6 and 5.1%, respectively. C-reactive protein was a significant factor associated with the presence of hematuria (OR [95% CI] 1.17 [1.03-1.34], p = 0.0194). The cumulative mortality was significantly higher in patients with hematuria alone (51.1%), proteinuria alone (47.1%), and both (66.7%), than in those with neither (24.3%). Moreover, the presence of hematuria alone was significantly associated with all-cause mortality (hazard ratio [95% CI] 1.78 [1.10-3.50], p = 0.0455), and patients with concomitant proteinuria were at the highest risk (4.01 [1.71-8.33], p = 0.0001). CONCLUSIONS: In patients with hematuric NHL, systemic inflammation is likely to develop to such a great extent that kidney damage occurs. Therefore, the presence of hematuria, alone or especially in combination with proteinuria, predicts a poor prognosis of NHL.

Autosomal Dominant Polycystic Kidney Disease with Emphysematous Polycystic Renal Infection That Required Surgical Treatment.

We encountered a patient with autosomal dominant polycystic kidney disease (ADPKD) complicated with emphysematous polycystic renal infection (EPRI). A 44-year-old woman visited our hospital for a fever, appetite loss, and gross hematuria. Because the patient was suffering from end-stage renal disease (ESRD), she was immediately hospitalized for hemodialysis. Multiple emphysematous infected cysts were noted in the right kidney, and antibiotic therapy and three rounds of cystic drainage were performed. However, the patient did not respond to treatment. Therefore, laparoscopic right nephrectomy was performed. ADPKD with comorbid EPRI is unresponsive to conservative treatment, and we believe that nephrectomy should be considered.

Anticentromere Antibody-positive Scleroderma Renal Crisis Requiring Dialysis.

A 70-year-old man with prior Raynaud's phenomena developed hypertension and renal insufficiency. Raynaud's phenomena, finger skin thickening, interstitial lung disease, and positive anticentromere antibody findings indicated systemic sclerosis (SSc). Based on the presence of SSc, severe hypertension with rapidly progressive renal failure, and proliferative and obliterative arteriolar vasculopathy, scleroderma renal crisis (SRC) was diagnosed. Despite good blood pressure control with antihypertensive drugs, hemodialysis was initiated and could not be withdrawn owing to unimproved renal dysfunction. Although SRC in anticentromere antibody-positive limited cutaneous SSc is extremely rare, some patients may develop SRC, and their renal prognosis may be poor.

Prevalence and mortality of chronic kidney disease in lymphoma patients: A large retrospective cohort study.

In patients with lymphoma, an important issue that has been recognized is renal involvement, including glomerulonephritis, acute kidney injury, and lymphoma infiltrating the kidney. However, the prevalence and mortality of chronic kidney disease (CKD) have not been fully understood in lymphoma patients. This study aimed to evaluate the prevalence of CKD and its impact on mortality in those patients.This was a retrospective cohort study of 429 consecutive lymphoma patients who were admitted or regularly visited our hospital from January 2013 to October 2016. CKD was defined as estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m and/or proteinuria ≥ 1+ that was sustained for at least 3 months. The prevalence of CKD at enrollment was evaluated according to the modified CKD classification by Kidney Disease: Improving Global Outcomes (KDIGO) (eGFR and proteinuria category). Dipstick proteinuria was classified into 3 grades: A1 for - and ±; A2 for 1+ or 2+; and A3 for ≥3+. The eGFR (mL/min/1.73 m) was classified into 6 stages: G1 for ≥90, G2 for 60 to 89, G3a for 45 to 59, G3b for 30 to 44, G4 for 15 to 29, and G5 for <15. The cumulative mortality rate was estimated using the Kaplan-Meier method, with stratification into 2 groups based on the presence or absence of CKD. Furthermore, a multivariate Cox proportional hazards regression model was used to calculate the hazard ratio (HR) and its 95% confidence interval (CI) for all-cause mortality, after adjustments for age, sex, pathologic type, clinical stage of lymphoma, presence or absence of diabetes mellitus, hypertension, and cardiovascular disease.The mean follow-up period was 3.06 ±â€Š0.96 years, and the prevalence of CKD at study enrollment was 34.5%. The cumulative mortality rate was 20.7%, and was significantly higher in the CKD group than in the group without CKD (36.4% vs 18.0%, P = .02). Multivariate analysis found mortality to be significantly associated with CKD (HR 1.58; 95% CI, 1.01-2.46), and this association was the most robust with very high-risk CKD (HR 6.94; 95% CI, 2.50-17.33).The prevalence of CKD in lymphoma patients was high. CKD should be considered an independent risk factor for mortality among patients with lymphoma.

Myeloperoxidase-antineutrophil cytoplasmic antibody causes different renal diseases by immune-complex formation and pauci-immune mechanism: A case report.

Antineutrophil cytoplasmic antibody (ANCA) has been known to cause pauci-immune crescentic glomerulonephritis. In addition, several reports described membranous glomerulonephritis (MN) concurrent with ANCA-associated glomerulonephritis. Because the two glomerular diseases simultaneously appear in an ANCA-positive patient, the mechanisms whereby ANCA causes the two different glomerular diseases remain ambiguous. Herein, we report a case of 19-year-old man who presented with hematuria, pre-nephrotic proteinuria, and high titer of myeloperoxidase (MPO)-ANCA. The first renal biopsy revealed MN with chronic glomerular scar lesions of unknown etiology. Predominant immunoglobulin (Ig) G1 subclass and negative phospholipase-A2 receptor staining, together with granular-positive glomerular capillary co-localization of MPO and IgG staining, suggested secondary MN due to MPO-MPO-ANCA immune-complex. Five years later, the patient presented with fever, severe renal dysfunction, and alveolar hemorrhage with high titer of MPO-ANCA that indicated pulmonary renal syndrome due to ANCA-associated vasculitis. The second renal biopsy revealed pauci-immune crescentic glomerulonephritis without either apparent MN-lesion or glomerular IgG staining. This is the first reported case showing that MPO-ANCA caused two different glomerular diseases, MN and pauci-immune crescentic glomerulonephritis, in the same patient at the different time points. Our case indicated that common MPO-ANCA might cause different glomerular diseases by different immune mechanisms.

A case of PR3-ANCA-positive anti-GBM disease associated with intrarenal arteritis and thrombotic microangiopathy.

Coexistence of anti-glomerular basement membrane (anti-GBM) disease with anti-neutrophil cytoplasmic antibody (ANCA) is occasionally reported and termed "double positive" disease. Interestingly, the majority of "double positive" ANCA is myeloperoxidase (MPO)-ANCA, and some of the MPO-ANCA-positive cases reveal intrarenal arteritis indicating an ANCA-associated renal lesion. In contrast, proteinase 3 (PR3)-ANCA-positive "double positive" disease had rarely been reported, and as far as we know, none of the cases showed intrarenal arteritis. Herein, we report a case of PR3-ANCA-positive "double positive" anti-GBM disease presenting with pulmonary-renal syndrome and hemolytic uremic syndrome. The kidney biopsy showed crescentic glomerulonephritis, intrarenal arteritis, and thrombotic microangiopathy. This case newly describes PR3-ANCA-associated intrarenal arteritis in "double positive" anti-GBM disease.

Bucillamine-induced membranous nephropathy with crescent formation in a patient with rheumatoid arthritis: case report and literature review.

Bucillamine is a disease-modifying antirheumatic drug that is structurally similar to D-penicillamine. The major renal side effect of bucillamine and D-penicillamine is proteinuria caused by membranous nephropathy (MN). In addition to MN, combined crescent formation has been occasionally reported in D-penicillamine-induced MN, while crescent formation has been rarely reported in bucillamine-treated cases. Here, we describe a 76-year-old female who presented with nephrotic syndrome and rapidly progressive glomerulonephritis. She was receiving bucillamine as initial treatment for recently diagnosed rheumatoid arthritis, and renal biopsy showed MN with crescent formation. To the best of our knowledge, this is the first report of bucillamine-induced MN with crescent formation in the English literature.

Renal infarction in a patient with pulmonary vein thrombosis after left upper lobectomy.

A 43-year-old male experienced renal infarction (RI) following left upper lobectomy for lung cancer. The patient complained of acute-onset severe left flank pain on the 14th postoperative day. A contrast-enhanced computed tomography (CT) of the abdomen revealed RI by a large wedge-shaped defect in the left kidney. A chest CT scan located the thrombus in the stump (a blind-ended vessel) of the left superior pulmonary vein. Therefore, thromboembolic RI caused by pulmonary vein thrombosis was suspected. Anticoagulation therapy was initiated with heparin and warfarin to treat RI and to prevent further embolic episodes. Two months later, pulmonary vein thrombosis had resolved without the appearance of additional peripheral infarction. This case emphasizes the need to consider thrombus in the stump of the pulmonary vein as a cause of RI.