Intravenous cyclophosphamide is considered to be the standard of care for the treatment of proliferative lupus nephritis. However, its use is limited by potentially severe toxic effects. Cyclosporine A has been suggested to be an efficient and safe treatment alternative to cyclophosphamide. Forty patients with clinically active proliferative lupus nephritis were randomly assigned to one of two sequential induction and maintenance treatment regimens based either on cyclophosphamide or Cyclosporine A. The primary outcomes were remission (defined as normal urinary sediment, proteinuria <0.3 g/24 h, and stable s-creatinine) and response to therapy (defined as stable s-creatinine, 50% reduction in proteinuria, and either normalization of urinary sediment or significant improvement in C3) at the end of induction and maintenance phase. Secondary outcomes were incidence of adverse events, and relapse-free survival. At the end of the induction phase, 24% of the 21 patients treated by cyclophosphamide achieved remission, and 52% achieved response, as compared with 26% and 43%, respectively of the 19 patients treated by the Cyclosporine A. At the end of the maintenance phase, 14% of patients in cyclophosphamide group, and 37% in Cyclosporine A group had remission, and 38% and 58% respectively response. Treatment with Cyclosporine A was associated with transient increase in blood pressure and reversible decrease in glomerular filtration rate. There was no significant difference in median relapse-free survival. In conclusion, Cyclosporine A was as effective as cyclophosphamide in the trial of sequential induction and maintenance treatment in patients with proliferative lupus nephritis and preserved renal function.(ClinicalTrials.gov identifier: NCT00976300)

Objective To evaluate the extended follow-up of the CYCLOFA-LUNE trial, a randomized prospective trial comparing two sequential induction and maintenance treatment regimens for proliferative lupus nephritis based either on cyclophosphamide (CPH) or cyclosporine A (CyA). Patients and methods Data for kidney function and adverse events were collected by a cross-sectional survey for 38 of 40 patients initially randomized in the CYCLOFA-LUNE trial. Results The median follow-up time was 7.7 years (range 5.0-10.3). Rates of renal impairment and end-stage renal disease, adverse events (death, cardiovascular event, tumor, premature menopause) did not differ between the CPH and CyA group, nor did mean serum creatinine, 24 h proteinuria and SLICC damage score at last follow-up. Most patients in both groups were still treated with glucocorticoids, other immunosuppressant agents and blood pressure lowering drugs. Conclusion An immunosuppressive regimen based on CyA achieved similar clinical results to that based on CPH in the very long term.

Introduction: Our study aimed to analyze whether renal parameters can predict mortality from COVID-19 disease in hospitalized patients. Methods: This retrospective cohort includes all adult patients with confirmed COVID-19 disease who were consecutively admitted to the tertiary hospital during the four-month period (1.9. - 31.12.2020). We analyzed their basic laboratory values, urinalysis, comorbidities, length of hospitalization, and survival. The RIFLE and KDIGO criteria were used for AKI and CKD grading, respectively. To display renal function evolution and the severity of renal damage, we subdivided patients further into 6 groups as follows: group 1 (normal renal function), group 2 (CKD grade 2+3a), group 3 (AKI-DROP defined as whose s-Cr dropped by >33.3% during the hospitalization), group 4 (CKD 3b), group 5 (CKD 4+5) and group 6 (AKI-RISE defined as whose s-Cr was elevated by ≥ 50% within 7 days or by ≥26.5 μmol/L within 48-hours during hospitalization). Then, we used eGFR on admission independently of renal damage to check whether it can predict mortality. Only 4 groups were used: Group I – normal renal function (eGFR>1.5 ml/s), group II mild renal involvement (eGFR 0.75-1.5), group III - moderate (eGFR 0.5-0.75) and group IV – severe (GFR<0.5). Results: 680 patients were included in our cohort. 244 patients displayed normal renal function, 207 patients fulfilled AKI, and 229 patients suffered from CKD. In total, a significantly higher mortality rate was found in the AKI and the CKD groups vs. normal renal function - 37.2% and 32.3% vs. 9.4%, respectively (P<0.001). In addition, the groups 1-6 divided by severity of renal damage reported mortality as 9.4%, 21.2%, 24.1%, 48.7%, 62.8% and 55.1%, respectively (P<0.001). The mean hospitalization duration of alive patients with normal renal findings was 9.5 days, while 12.1 days in patients with any renal damage (P<0.001). When all patients were compared according to eGFR on admission, the mortality was as follows: Group I (normal) 9.8%, Group II (mild) 22.1%, group III (moderate) 40.9% and group IV (severe) 50.5%, respectively (P<0.001). It was a significantly better mortality predictor than CRP on admission (AUC 0.7053 vs. 0.6053). Conclusions: Mortality in patients with abnormal renal function was 3 times higher compared to patients with normal renal function. Also, patients with renal damage had a worse and longer hospitalization course. Lastly, eGFR on admission, independently of any renal damage, was an excellent tool for predicting mortality. Further, the change in s-Cr levels during hospitalization reflected the mortality prognosis.

Genetic polymorphisms in serotonergic receptors 5 and cytochrome-P450 enzymes (such as CYP2D6) may also heighten the serotonergic response. This patient may possess more-sensitive serotonergic receptors, less-active cytochrome enzymes, or both. In addition, the elimination of nor-fluoxetine and duloxetine is through the kidneys. The normal age-related decline of glomerular filtration 6 in elderly people would lengthen the retention of fluoxetine and norfluoxetine. In addition, CNS hyperactivity from high synaptic norepinephrine concentrations has been shown to correlate with serotonin syndrome, 7 and duloxetine, an SNRI, can raise the synaptic norepinephrine level.Depression is common in elderly people, and the drugs of choice for major depressive disorder in elderly people are SSRIs. 8 With fluoxetine being the second most prescribed generic SSRI in the United States 9 and duloxetine gaining popularity for treatment of depression, this type of case may recur. Considering the decline of kidney function in elderly people and the long half-life of SSRIs, physicians should make dose adjustment for SSRIs in elderly people and wait for a wash-out period before starting another SSRI or an SNRI. Geriatricians should know that serotonin syndrome may occur not only from the combined use of SSRIs and SNRIs, but also during a shift from an SSRI to an SNRI.

Anticoagulation-related nephropathy (ARN) is a significant and underdiagnosed complication in patients who receive anticoagulation therapy. It is characterized by acute kidney injury in the setting of excessive anticoagulation defined as an international normalized ratio > 3.0 in patients treated with warfarin. A definitive diagnosis is made by renal biopsy showing acute tubular necrosis with obstruction of the tubuli by red blood cell casts. However, the evidence shows that ARN can occur during treatment with novel oral anticoagulants as well. Although it has been suggested that antiplatelet therapy, such as aspirin, might contribute to coagulopathy (and therefore the hypothetical risk of ARN), there are no reports of ARN induced by antiplatelet therapy according to our knowledge. It is also reported that glomerular lesions (i.e., kidney disease) represent a risk factor for ARN. We present a case of an 82-year-old man who developed biopsy-proven ARN after the administration of dual antiplatelet therapy with no previous anticoagulation treatment and normal coagulation tests.