Clinicopathological features and prognosis of kidney injury in patients after hematopoietic stem cell transplantation / 中华预防医学杂志

To summarize the clinicopathological features and prognosis of kidney injury after hematopoietic stem cell transplantation (HSCT), to provide basis for preventing its occurrence and development. By using a retrospective cohort study method, we collected the clinical and renal biopsy pathological data of all the patients who hospitalized in the Department of Nephrology of Peking University First Hospital from June 2011 to June 2021 with renal injury after HSCT and underwent renal biopsy, and prognosis was followed up by telephone. The clinical laboratory characteristics, renal pathology and prognosis, and their association were analyzed. The results showed that the most common clinical phenotype was chronic kidney disease (CKD,69.2%, 18/26), in this term 13/18 patients received stem cells from haploidentical donors, and 11/18 patients experienced with extrarenal graft-versus-host disease (GVHD). The most common pathologic phenotype was thrombotic microangiopathy (TMA, 61.5%, 16/26). Renal function returned to baseline level in 6 patients, and the kidney survival at 2 years and 5 years were 95.7% (22/23) and 87.5% (14/16), respectively. In conclusion, the clinical phenotype of renal injury after HSCT were mainly CKD, and the most common pathologic phenotype was TMA, the long-term prognosis was favourable.

Paraquat-induced Thrombotic Microangiopathy: The Pathophysiology in Hyperacute Paraquat Poisoning Deaths / Microangiopatía trombótica inducida por paraquat: fisiopatología de las muertes por envenenamiento hiperagudo con paraquat

ABSTRACT This paper described the pathophysiology of suicide deaths from paraquat poisoning which occurred in patients who died in fewer than 24 hours after ingesting paraquat. These deaths were referred to as hyperacute paraquat poisoning deaths. Thrombotic microangiopathy was the predominant pathological finding in all these cases and was evident in the brain, lung, heart, kidneys and in all organs and tissues examined. Of note, diffuse alveolar capillary thrombosis occurred, causing damage to alveolar walls, including those in subpleural locations, resulting in focal visceral pleural rupture leading to pneumothorax and pneumomediastinum in these cases, thus giving rise to yet another mechanism of pneumothorax and pneumomediastinum in paraquat toxicity. Thrombotic microangiopathy is the major pathological mechanism that underlies paraquat poisoning and has not hitherto been reported.

RESUMEN El presente trabajo describe la fisiopatología de las muertes por suicidio por intoxicación con paraquat en pacientes que murieron en menos de 24 horas después de ingerirlo. Estas muertes fueron referidas como muertes por envenenamiento hiperagudo con paraquat. La microangiopatía trombótica fue el hallazgo patológico predominante en todos estos casos, y se hizo evidente en el cerebro, el pulmón, el corazón, los riñones y en todos los órganos y los tejidos examinados. Es de notar que se produjo una trombosis capilar alveolar difusa, que causó daño a las paredes alveolares, incluyendo aquellas en localizaciones subpleurales. Esto trajo como resultado la ruptura pleural visceral focal que condujo al neumotórax y al neumomediastino en estos casos, dando así lugar a otro mecanismo de neumotórax y neumomediastino en la toxicidad del paraquat. La microangiopatía trombótica es el mecanismo patológico principal que subyace en el envenenamiento por paraquat, y no ha sido reportada hasta el momento.

Síndrome nefrótico e injuria renal aguda con microangiopatía trombótica en mujer con enfermedad celíaca: Caso clínico / Nephrotic syndrome and acute kidney injury associated with celiac disease: Report of one case

Celiac disease may be associated with other autoimmune diseases and exceptionally with glomerulopathies and nephrotic syndrome. Associations have been reported with IgA nephropathy, membranoproliferative glomerulonephritis, membranous glomerulopathy and minimal change disease. We report a 63-year-old woman who simultaneously presented with massive nephrotic syndrome (proteinuria 46 g/day) and cachexia due to a malabsorption syndrome secondary to celiac disease. The course of her diseases was complicated with cardiomyopathy due to severe malnutrition, septic shock, acute kidney injury that required dialysis for seven weeks and severe hypertension. A renal biopsy showed a membranoproliferative pattern of injury secondary to a thrombotic microangiopathy and diffusepodocyte damage. Fouryears later, the patient was in good general health, the glomerular filtration rate was 30 ml/min/1.73m² and there was non-nephrotic proteinuria.

Viral-associated thrombotic microangiopathies

Thrombotic microangiopathies encompass a group of disorders characterized by microangiopathic he-molytic anemia, thrombocytopenia associated with hyaline thrombi [comprised primarily of platelet aggregates in the microcirculation], and varying degrees of end-organ failure. Many primary [genetic] and secondary etiological predisposing factors have been describednamely pregnancy, autoimmune disorders, cancer, drugs and antineoplastic therapy, bone marrow transplantation/solid organ transplantation, and infections. In the setting of infectious diseases, the association with Shiga or Shiga-like exotoxin of Escherichia coli 0157:H7 or Shigella dysenteriae type 1-induced typical hemolytic uremic syndrome is well known. Recently however, an increasing body of evidence suggests that viruses may also play an important role as trigger factors in the pathogenesis of thrombotic microangiopathies. This is a comprehensive review focusing on the current understanding of viral associated/induced endothelial stimulation and damage that ultimately leads to the development of this life-threatening multisystemic disorder