D ifferential diagnosis of primary IgA nephropathy (IgAN) and IgA-dominant infection-related glomerulonephritis, particularly Staphylococcus infectionÀassociated glomerulonephritis (SAGN), on a kidney biopsy sample can be challenging because of similar morphologic findings by light microscopy, immunofluorescence, and

Tacrolimus monotherapy is an effective and safe option for the treatment of MN with stable renal function. Relapses are frequent in patients with PR and can be partially prevented by a longer tapering period.

The addition of spironolactone or hydrochlorothiazide enhances the antialbuminuric effect of renin-angiotensin blockers. However, comparative studies on the effect of different diuretics are lacking. We conducted a prospective randomized crossover study to compare the effects of spironolactone (25 mg/day), hydrochlorothiazide (50 mg/day) without/with amiloride (5 mg/day) on top of enalapril treatment in 21 patients with CKD stages 1-3 and a urinary albumin-to-creatinine ratio (UACR) over 300 mg/g. Treatment periods lasted 4 weeks. The UACR showed a significant reduction with the diuretics: spironolactone, -34% or hydrochlorothiazide without/with amiloride -42% or -56%, respectively. Reduction of the UACR was significantly greater with hydrochlorothiazide without/with amiloride when compared with spironolactone. The percentage of patients who achieved UACR reductions greater than 30% and 50% was greater with hydrochlorothiazide without/with amiloride (81% and 57%, and 81% and 66%, respectively) when compared with spironolactone alone (57% and 28%, respectively). Glomerular filtration rate (GFR), blood pressure, and body weight decreased with the three diuretic regimens. A significant correlation was found between the UACR reduction and GFR and blood pressure changes. Thus, diverse diuretic regimens differentially enhance albuminuria reduction, an effect likely associated with the degree of GFR reduction.

Aldosterone antagonist treatment in obese patients with proteinuric nephropathies induces a drastic and sustained reduction in proteinuria but not more than the non-obese group. There was a trend toward slowing progression of renal failure with few adverse events.

<b><i>Background:</i></b> Although diuretics are one of the most widely used drugs by nephrologists, their antiproteinuric properties are not generally taken into consideration. <b><i>Summary:</i></b> Thiazide diuretics have been shown to reduce proteinuria by &#x3e;35% in several prospective controlled studies, and these values are markedly increased when combined with a low-salt diet. Thiazide-like diuretics (indapamide and chlorthalidone) have shown similar effectiveness. The antiproteinuric effect of mineralocorticoid receptor antagonists (spironolactone, eplerenone, and finerenone) has been clearly established through prospective and controlled studies, and treatment with finerenone reduces the risk of chronic kidney disease progression in type-2 diabetic patients. The efficacy of other diuretics such as amiloride, triamterene, acetazolamide, or loop diuretics has been less explored, but different investigations suggest that they might share the same antiproteinuric properties of other diuretics that should be evaluated through controlled studies. Although the inclusion of sodium-glucose cotransporter-2 inhibitors (SGLT2i) among diuretics is a controversial issue, their renoprotective and cardioprotective properties, confirmed in various landmark trials, constitute a true revolution in the treatment of patients with kidney disease. Recent subanalyses of these trials have shown that the early antiproteinuric effect induced by SGLT2i predicts long-term preservation of kidney function. <b><i>Key Message:</i></b> Whether the early reduction in proteinuria induced by diuretics other than finerenone and SGLT2i, as summarized in this review, also translates into long-term renoprotection requires further prospective and observational studies. In any case, it is important for the clinician to be aware of the antiproteinuric properties of drugs so often used in daily clinical practice.

The development of drugs capable of modulating angiogenesis has created a significant improvement in the survival associated with metastatic tumors. This group of drugs includes anti-vascular endothelial growth factor (VEGF) monoclonal antibodies (bevacizumab), intracellular VEGF receptor inhibitors (sorafenib, sutinib, pazopanib), and the small VEGF inactivating molecules (VEGF trap).1 The most frequent renal side effect involvement is arterial hypertension, proteinuria, and thrombotic microangiopathy (TMA).1-4 However, there is little information available regarding the relationship between these drugs and the development of malignant hypertension (MHT).2,3 Here we present two patients with clear cell renal carcinoma treated with VEGF inhibitors who developed MHT.The first case was a 46-year-old woman diagnosed with clear cell renal carcinoma treated with a left radical nephrectomy. Five months after surgery she began treatment with pazopanib because of the appearance of metastasis. Three weeks after starting treatment she presented to the emergency department with blurry vision and headache. Physical examination revealed a blood pressure (BP) of 220 ⁄ 110 mm Hg and retinal examination revealed multiple cotton-wool spots, retinal hemorrhages, and swelling of the optic disk (grade IV hypertensive retinopathy). Results of laboratory tests revealed a serum creatinine (SCr) level of 1.3 mg ⁄ dL and proteinuria of 1.5 g ⁄ 24 hours with normal sediment, and hemogram results showed a thrombopenia of 99,000 platelets, with a hemoglobin level of 12 g ⁄ dL. To control BP the following were used: a b-blocker, calcium channel blockers, angiotensin-converting enzyme (ACE) inhibitors, and a-blockers, which achieved a BP of 120 ⁄ 60 mm Hg. Pazopanib was suspended until BP was controlled and re-introduced without complications. Renal function improved with creatinine of 0.9 mg ⁄ dL upon hospital discharge and negative proteinuria in the 24-hour analysis.The second case was a 53-year-old woman with a history of hypertension and clear cell renal carcinoma with pleural metastases treated with a left radical nephrectomy. After surgery she began treatment with sunitinib. Two months later the patient was admitted to the nephrology department for a hypertensive crisis and acute renal failure. Upon arrival, her BP was 180 ⁄ 100 mm Hg, she revealed grade III hypertensive retinopathy, and hemogram showed a hemoglobin level of 8.4 g ⁄ dL, 53,000 platelets, and schistocytes in the peripheral blood. The biochemical studies showed lactate dehydrogenase 798 U ⁄ L, SCr 4.3 mg ⁄ dL, and proteinuria 5 to 6 g ⁄ 24 hours. The patient was prescribed valsartan, enalapril, and amlodipine to control BP. With the clinical diagnosis of MHT and TMA, and in view of the seriousness of acute renal failure, she was taken off the drug and started on hemodialysis and plasmapheresis (5 sessions) without satisfactory results, continuing a program of chronic renal replacement treatment.VEFG is a powerful promoter of angiogenesis and is produced by different tum...

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Kidney transplantation is the best option for patients with end-stage renal disease. Despite the improvement in cardiovascular burden (leading cause of mortality among patients with chronic kidney disease), cardiovascular adverse outcomes related to the inflammatory process remain a problem. Thus, the aim of the present study was to characterize the immune profile and microvesicles of patients who underwent transplantation. We investigated the lymphocyte phenotype (CD3, CD4, CD8, CD19, and CD56) and monocyte phenotype (CD14, CD16, CD86, and CD54) in peripheral blood, and endothelium-derived microvesicles (annexin V+CD31+CD41–) in plasma of patients with advanced chronic kidney disease (n = 40), patients with transplantation (n = 40), and healthy subjects (n = 18) recruited from the University Hospital “12 de Octubre” (Madrid, Spain). Patients with kidney transplantation had B-cell lymphopenia, an impairment in co-stimulatory (CD86) and adhesion (CD54) molecules in monocytes, and a reduction in endothelium-derived microvesicles in plasma. The correlations between those parameters explained the modifications in the expression of co-stimulatory and adhesion molecules in monocytes caused by changes in lymphocyte populations, as well as the increase in the levels of endothelial-derived microvesicles in plasma caused by changes in lymphocyte and monocytes populations. Immunosuppressive treatment could directly or indirectly induce those changes. Nevertheless, the particular characteristics of these cells may partly explain the persistence of cardiovascular and renal alterations in patients who underwent transplantation, along with the decrease in arteriosclerotic events compared with advanced chronic kidney disease. In conclusion, the expression of adhesion molecules by monocytes and endothelial-derived microvesicles is related to lymphocyte alterations in patients with kidney transplantation.