RESUMO
Across the globe, the frequent occurrence of drought spells has significantly undermined the sustainability of modern high-input farming systems, particularly those focused on staple crops like wheat. To ameliorate the deleterious impacts of drought through a biologically viable and eco-friendly approach, a study was designed to explore the effect of nicotinic acid on different metabolic, and biochemical processes, growth and yield of wheat under optimal moisture and drought stress (DS). The current study was comprised of different levels of nicotinic acid applied as foliar spray (0 g L-1, 0.7368, 1.477, 2.2159 g L-1) and fertigation (0.4924, 0.9848, and 1.4773 g L-1) under normal conditions and imposed drought by withholding water at anthesis stage. The response variables were morphological traits such as roots and shoots characteristics, yield attributes, grain and biological yields along with biosynthesis of antioxidants. The results revealed that nicotinic acid dose of 2.2159 g L-1 out-performed rest of treatments under both normal and DS. The same treatment resulted in the maximum root growth (length, fresh and dry weights, surface area, diameter) and shoot traits (length, fresh and dry weights) growth. Additionally, foliar applied nicotinic acid (2.2159 g L-1) also produced as the highest spike length, grains spike-1, spikelet's spike-1 and weight of 1000 grains. Moreover, these better yield attributes led to significantly higher grain yield and biological productivity of wheat. Likewise in terms of physiological growth of wheat under DS, the same treatment remained superior by recording the highest SPAD value, relative water content, water potential of leaves, leaf area, stomatal conductance (292 mmolm-2S-1), internal carbon dioxide concentration, photosynthesis and transpiration rate. Interestingly, exogenously applied nicotinic acid remained effective in triggering the antioxidant system of wheat by recording significantly higher catalase, peroxidase, superoxide dismutase and ascorbate peroxidase.
Assuntos
Antioxidantes , Niacina , Antioxidantes/metabolismo , Triticum/metabolismo , Secas , Água/metabolismo , Grão Comestível/metabolismo , Mecanismos de DefesaRESUMO
Thrombotic microangiopathy (TMA) is an uncommon but serious complication that not only affects native kidneys but also transplanted kidneys. This review is specifically focused on post-transplant TMA (PT-TMA) involving kidney transplant recipients. Its reported prevalence in the latter population varies from 0.8% to 14% with adverse impacts on both graft and patient survival. It has many causes and associations, and the list of etiologic agents and associations is growing constantly. The pathogenesis is equally varied and a variety of patho genetic pathways lead to the development of microvascular injury as the final common pathway. PT-TMA is categorized in many ways in order to facilitate its management. Ironically, more than one causes are contributory in PT-TMA and it is often difficult to pinpoint one particular cause in an individual case. Pathologically, the hallmark lesions are endothelial cell injury and intravascular thrombi affecting the microvasculature. Early diagnosis and classification of PT-TMA are imperative for optimal outcomes but are challenging for both clinicians and pathologists. The Banff classification has addressed this issue and has developed minimum diagnostic criteria for pathologic diagnosis of PT-TMA in the first phase. Management of the condition is also challenging and still largely empirical. It varies from simple maneuvers, such as plasmapheresis, drug withdrawal or modification, or dose reduction, to lifelong complement blockade, which is very expensive. A thorough understanding of the condition is imperative for an early diagnosis and quick treatment when the treatment is potentially effective. This review aims to increase the awareness of relevant stakeholders regarding this important, potentially treatable but under-recognized cause of kidney allograft dysfunction.
RESUMO
The second half of the previous century witnessed a tremendous rise in the number of clinical kidney transplants worldwide. This activity was, however, accompanied by many issues and challenges. An accurate diagnosis and appropriate management of causes of graft dysfunction were and still are, a big challenge. Kidney allograft biopsy played a vital role in addressing the above challenge. However, its interpretation was not standardized for many years until, in 1991, the Banff process was started to fill this void. Thereafter, regular Banff meetings took place every 2 years for the past 30 years. Marked changes have taken place in the interpretation of kidney allograft biopsies, diagnosis, and classification of rejection and other non-rejection pathologies from the original Banff 93 classification. This review attempts to summarize those changes for increasing the awareness and understanding of kidney allograft pathology through the eyes of the Banff process. It will interest the transplant surgeons, physicians, pathologists, and allied professionals associated with the care of kidney transplant patients.
RESUMO
BACKGROUND: Proteinuria is an important and well-known biomarker of many forms of kidney injury. Its quantitation is of particular importance in the diagnosis and management of glomerular diseases. Its quantification can be done by several methods. Among these, the measurement of 24-h urinary protein excretion is the gold standard method. However, it is cumbersome, time-consuming, and inconvenient for patients and is not completely foolproof. Many alternative methods have been tested over time albeit with conflicting results. Among the latter, the measurement of urine protein-to-creatinine ratio (uPCR) in single-voided urinary samples is widely used. The majority of studies found a good correlation between uPCR in single urine samples with 24-h urinary protein estimation, whereas others did not. AIM: To investigate the correlation of spot uPCR with 24-h urinary protein estimation in patients suffering from different forms of glomerulopathies at a single large-volume nephrological center in Pakistan. METHODS: This cross-sectional, observational study was conducted at the Department of Nephrology, Sindh Institute of Urology and Transplantation, Karachi, Pakistan from September 2017 to March 2018. All newly presenting adult patients with proteinuria who were being investigated for suspected glomerulonephritis and persistent proteinuria with ages between 18 to 60 years were enrolled. All patients were given detailed advice regarding 24-h urine collection starting at 7:00 AM for total protein and creatinine excretion estimations. A spot urine sample was collected the next day at the time of submission of a 24-h urine sample for measuring uPCR along with a blood sample. The data of patients were collected in a proforma. SPSS version 20.0 was used for statistical analysis. RESULTS: A total of 157 patients were included. Their mean age was 30.45 ± 12.11 years. There were 94 (59.8%) males and 63 (40.2%) females. The mean 24-h urinary protein excretion was 3192.78 ± 1959.79 mg and the mean spot uPCR was 3.16 ± 1.52 in all patients. A weak but significant correlation was observed between spot uPCR and 24-h urinary protein excretion (r = 0.342, P = 0.01) among all patients. On subgroup analysis, a slightly better correlation was found in patients older than 47 years (r = 0.78), and those with body mass index > 25 kg/m2 (r = 0.45). The Bland and Altman's plot analysis comparing the differences between spot uPCR and 24-h protein measurement also showed a wide range of the limits of agreement between the two methods. CONCLUSION: Overall, the results from this study showed a significant and weakly positive correlation between spot uPCR and 24-h urinary protein estimation in different forms of glomerulopathies. The agreement between the two methods was also poor. Hence, there is a need for careful interpretation of the ratio in an unselected group of patients with kidney disease.