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Metodo Se efectuo una busqueda en las bases de datos Central Cochrane, Embase, Google Scholar, OvidMedline, ProQuest y Scopus de articulos publicados entre 2013 y 2025 que informaran sobre la incidencia, etiologia y desenlaces de esta afeccion en paises de ingresos bajos y medianos. Se llevo a cabo un metanalisis de los estudios que utilizaron los criterios diagnosticos de la organizacion Kidney Disease: Improving Global Outcomes. Se realizaron analisis por subgrupos y una metarregresion para explorar fuentes de heterogeneidad. [phrase omitted]

Preeclampsia is a disorder that can occur during pregnancy and is one of the leading causes of death among pregnant women. This disorder occurs after the 20th week of pregnancy and is characterized by arterial hypertension, proteinuria, fetoplacental, and multiple organ dysfunctions. Despite the long history of studying preeclampsia, its etiology and pathogenesis remain poorly understood, and therapy is symptomatic. One of the factors of the disorder is believed to be misfolded proteins that are prone to form amyloid aggregates. The CRD tests, utilizing the binding of the amyloid-specific dye Congo red to urine components, demonstrate high efficiency in diagnosing preeclampsia. However, these tests have also been found to be positive in other disorders with proteinuria, presumably associated with concomitant amyloidosis. To assess the limitations of the CRD tests, we examined urine congophilia and protein components mediating Congo red positivity in patients with proteinuria, including preeclampsia, amyloid and non-amyloid nephropathies. We stained the urine samples and calculated congophilia levels. We also assessed the contribution of large protein aggregates to congophilia values using ultracentrifugation and determined the molecular weights of congophilic urinary proteins using centrifugal concentrators. All proteinuric groups demonstrate positive results in the CRD tests and congophilia levels were more than two times higher compared with the control non-proteinuric groups ( p <0.01). There was a strong correlation between urine protein excretion and congophilia in amyloid nephropathy ( r s = 0.76), non-amyloid nephropathies ( r s = 0.90), and preeclampsia ( r s = 0.90). Removal of large aggregates from urine did not affect the congophilia levels. Separation of urine protein fractions revealed congophilic components in the range of 30–100 kDa, including monomeric serum albumin. Our results indicate limitations of CRD tests in preeclampsia diagnostics in women with renal disorders and underscore the need for further research on the mechanisms of Congo red binding with urine components.

Objectives This study aimed to investigate the impact of pregnancy and pre-existing comorbidities on COVID-19 infections and associated complications of hospitalisation and mortality in women of reproductive age (WRA). The study also compared the risk of severe COVID-19 complications between pregnant women (PW) and non-pregnant women (NPW) with and without pre-existing comorbidities. Special focus was placed on some understudied comorbidities of immunosuppression, chronic renal disease and chronic obstructive pulmonary disease (COPD). Methods The study utilized anonymized patient-related information for a population of 7,342,869 WRA from the Mexican Ministry of Health data repository on COVID-19. Descriptive variables were characterized using frequencies, percentages, means, and standard deviations. Adjusted odds ratios (aORs) were used to assess the associations between risk factors and outcomes of hospitalisation and mortality. The study covered the entire COVID-19 pandemic period from January 30, 2020, to May 5, 2023. Results The findings revealed that PW were not more likely to get COVID-19 infections than NPW. PW with COVID-19 infections were more likely to require hospital admission, intubation treatments, and ICU admission compared to NPW with COVID-19. PW with immunosuppression had an increased odds ratio (aOR) of getting COVID-19 infections compared to NPW (PW: aOR = 1.0396; NPW: aOR = 0.8373). NPW with immunosuppression had higher risk of mortality (all-cause death: aOR = 1.7084; COVID-19-associated death: aOR = 1.4079) and hospitalisation (all-cause hospitalisation: aOR = 4.1328; COVID-19-associated hospitalisation: aOR = 3.0451) than NPW without immunosuppression. Renal disease was identified as a concerning pre-existing condition that increased the risks of COVID-19 associated mortality/hospitalizations and all-cause mortality/hospitalizations for both PW and NPW. NPW with renal disease had much higher odds ratio (aOR) of either COVID-19-associated-hospitalisations (NPW: aOR = 8.639; PW: aOR = 1.7603) or all-cause hospitalisations (NPW: aOR = 8.8594; PW: aOR = 1.786) than PW with renal disease. Conclusions This study provides valuable insights into the impact of pregnancy and pre-existing comorbidities on COVID-19 outcomes in WRA. The findings underscore the importance of considering demographic factors and pre-existing comorbidities in the management of PW with COVID-19. The study also highlights the need for further research to understand the unique impacts of different comorbidities, particularly immunosuppression and renal disease, on COVID-19 outcomes in WRA.

Preeclampsia (PE), the most severe presentation of hypertensive disorders of pregnancy, is the major cause of morbidity and mortality linked to pregnancy, affecting both mother and fetus. Despite advances in prophylaxis and managing PE, delivery of the fetus remains the only causative treatment available. Focus on complex pathophysiology brought the potential for new treatment options, and more conservative options allowing reduction of feto-maternal complications and sequelae are being investigated. Endogenous digitalis-like factors, which have been linked to the pathogenesis of preeclampsia since the mid-1980s, have been shown to play a role in the pathogenesis of various cardiovascular diseases, including congestive heart failure and chronic renal disease. Elevated levels of EDLF have been described in pregnancy complicated by hypertensive disorders and are currently being investigated as a therapeutic target in the context of a possible breakthrough in managing preeclampsia. This review summarizes mechanisms implicating EDLFs in the pathogenesis of preeclampsia and evidence for their potential role in treating this doubly life-threatening disease.

Diabetes mellitus complicates pregnancies, leading to diseases in adult life in the offspring. Asymmetric dimethylarginine (ADMA) is increased in diabetes mellitus, kidney disease, and hypertension. We tested whether maternal diabetes causes increased ADMA in rats, resulting in kidney disease and hypertension in the adult offspring, and whether these can be prevented by maternal citrulline supplementation. Newborn female and pregnant Sprague-Dawley rats were injected with streptozotocin (STZ), which made up the nSTZ and STZ models, respectively. For the STZ model, 4 groups of male offspring were killed at age 3 months: the control, STZ, and Cit and STZ+Cit (control and STZ rats treated with 0.25% l-citrulline solution, respectively) groups. The nSTZ rats had lower nephron numbers. The renal level of ADMA was higher in the nSTZ rats than in controls. The STZ group developed kidney injury, renal hypertrophy, and elevated blood pressure at the age of 12 weeks. These conditions were found to be associated with increased ADMA levels, decreased nitric oxide (NO) production, and decreased dimethylarginine dimethylaminohydrolase (DDAH) activity in the kidney. In addition, ADMA caused a nephron deficit in cultured rat metanephroi. Maternal citrulline supplementation prevented hypertension and kidney injury, increased the renal DDAH-2 protein level, and restored the levels of ADMA and NO in the STZ+Cit group. Reduced nephron number and increased ADMA contribute to adult kidney disease and hypertension in offspring of mothers with STZ-induced diabetes. Manipulation of the ADMA-NO pathway by citrulline supplementation may be a potential approach to prevent these conditions.

Thrombotic microangiopathy (TMA) is a clinical-pathological syndrome defined by microangiopathic hemolytic anemia, thrombocytopenia, and organ dysfunction, commonly affecting the kidneys. The etiologies are diverse and include genetic disorders (affecting complement proteins or other pathways, such as cobalamin metabolism), infections, autoimmune diseases, malignancies, transplantation, pregnancy, and drugs. Differentiating these causes is essential, as treatment strategies and prognoses vary widely. This consensus document, developed by a multidisciplinary group of clinicians and geneticists, provides a structured approach for evaluating TMA, with particular focus on complement-mediated TMA (C-TMA). C-TMA should be considered when TMA features persist after resolution or exclusion of secondary causes. Diagnostic confirmation relies on clinical judgment, histopathology, and a favorable response to C5 complement inhibitors, such as eculizumab or ravulizumab. This therapeutic response is considered both diagnostic and prognostic. Complement gene variants (e.g., CFH , CFI , MCP/CD46 , and others) and copy number variations (e.g., CFHR1-5 deletions) are found in up to 50–60% of patients, but their absence does not rule out C-TMA. Early complement inhibition may prevent irreversible organ damage and should not be delayed by pending genetic results. Genetic counseling is advised for all patients, regardless of variant status, to assess familial risk and guide long-term follow-up. A consensus aims to outline scenarios in which treatment initiation is strongly recommended, including severe or relapsing disease, chronic kidney dysfunction, among others. In Chile and Latin America, TMA remains underdiagnosed due to limited access to specialized diagnostic tools and delays in recognizing clinical subtypes. The availability of molecular testing and complement studies is restricted, often delaying targeted therapies. Treatment still relies heavily on plasma exchange, with limited access to complement inhibitors. This consensus aims to standardize care, improve early recognition, and support rational use of targeted therapies in C-TMA, particularly in regions with limited access to specialized testing or complement inhibitors.

In some cases, mitochondrial disease can remain undiagnosed until pregnancy reveals systemic symptoms. Clinicians should therefore consider this diagnosis in young patients presenting with diabetes, kidney disease, and hearing loss. Early diagnosis can improve maternal and fetal outcomes, particularly in high‐risk pregnancies complicated by unexplained preterm birth or cardiomyopathy.

Women with preeclampsia (PE) have a greater risk of developing hypertension, cardiovascular disease (CVD), and renal disease later in life. Angiotensin II type I receptor agonistic autoantibodies (AT1-AAs) are elevated in women with PE during pregnancy and up to 2-year postpartum (PP), and in the reduced uterine perfusion pressure (RUPP) rat model of PE. Blockade of AT1-AA with a specific 7 amino acid peptide binding sequence (‘n7AAc’) improves pathophysiology observed in RUPP rats; however, the long-term effects of AT1-AA inhibition in PP is unknown. Pregnant Sprague Dawley rats were divided into three groups: normal pregnant (NP) ( n  = 16), RUPP ( n  = 15), and RUPP + ‘n7AAc’ ( n  = 16). Gestational day 14, RUPP surgery was performed and ‘n7AAc’ (144 μg/day) administered via osmotic minipump. At 10-week PP, mean arterial pressure (MAP), renal glomerular filtration rate (GFR) and cardiac functions, and cardiac mitochondria function were assessed. MAP was elevated PP in RUPP vs. NP (126 ± 4 vs. 116 ± 3 mmHg, p  < 0.05), but was normalized in in RUPP + ‘n7AAc’ (109 ± 3 mmHg) vs. RUPP ( p  < 0.05). PP heart size was reduced by RUPP + ’n7AAc’ vs. RUPP rats ( p  < 0.05). Complex IV protein abundance and enzymatic activity, along with glutamate/malate-driven respiration (complexes I, III, and IV), were reduced in the heart of RUPP vs. NP rats which was prevented with ‘n7AAc’. AT1-AA inhibition during pregnancy not only improves blood pressure and pathophysiology of PE in rats during pregnancy, but also long-term changes in blood pressure, cardiac hypertrophy, and cardiac mitochondrial function PP.

Postpartum pulmonary syndrome as lupus flares in inactive or mild lupus is uncommon. The diagnosis and management of postpartum lupus flare in second pregnancy presenting with crescentic lupus nephritis (LN), secondary thrombotic microangiopathy (TMA), and severe lupus vasculitis in an undiagnosed systemic lupus erythematosus is extremely challenging. Here, in this case report, we present a young lady who presented with postpartum acute kidney injury (AKI) with systemic complaints about 4 weeks post-term uneventful delivery. Renal biopsy was suggestive of crescentic LN with severe lupus vasculitis. The stormy course was further complicated with diffuse alveolar hemorrhage, portal venous thrombosis, TMA, and anuric AKI requiring renal replacement therapy. She received multiple sessions of plasmapheresis, steroid, intravenous immunoglobulin, inj. cyclophosphamide, and started showing improvement after about 6 weeks of presentation.

A 34-year-old nulliparous gravid female presented with acute bilateral pyelonephritis at 29 + 5 weeks gestation. The patient was relatively well until two weeks ago when a slight increase in amniotic fluid was noted. Further investigation revealed myoglobinuria and significantly elevated levels of creatine phosphokinase. The patient was subsequently diagnosed with rhabdomyolysis. Twelve hours after admission, the patient noted reduced fetal movements. A non-stress test revealed fetal bradycardia and non-reassuring variability in fetal heart rate. An emergency cesarean section was performed, and a “floppy” female child was delivered. Genetic testing revealed congenital myotonic dystrophy, and the mother was also diagnosed with myotonic dystrophy. Rhabdomyolysis has a very low incidence in pregnancy. Herein, we report a rare case of myotonic dystrophy with rhabdomyolysis in a gravid female with no history of myotonic dystrophy. Acute pyelonephritis is a causative agent of rhabdomyolysis that results in preterm birth.