Renal replacement therapy in the form of renal transplantation (RT) is the treatment of choice in these patients. Various factors influence the graft survival, infections being most common. Infections account for 16% of patient deaths and 7.7% of death censored graft failure in renal transplant patients. Urinary tract infection (UTI) is the most common infectious complication accounting for 45–72% of all infections. According to few studies UTI may have a negative impact over the long term survival of renal allograft. There are multiple factors that predispose these patients to UTI. Elderly age group, female gender, increased duration of catheterization and anatomical abnormalities of the urinary tract are most common predisposing factors. E. coli is the most frequently isolated organisms from the urine of these patients. We would proceed further with two cases which presented as UTI in post-transplant period. The first patient transplanted (living donor related) for diabetes induced end stage renal disease had developed UTI 4 years post-transplant. The other patient underwent deceased donor renal transplant for adult polycystic disease related chronic kidney disease, presented 2 years post-transplant with UTI.
Part of the book: Urinary Tract Infection
Adrenal gland is an endocrine organ comprising of an outer cortex and inner medulla. These secrete various hormones that have a vital role in maintaining the normal homeostasis of the body. Lesions of adrenal cortex are quite common to encounter and most of these are related to the hormones secreted by three layers of adrenal cortex: the zona glomerulosa, the zona fasciculata, and the zona reticularis. Also it is very infrequent to encounter metastatic lesions in the adrenal glands too. So it is very important as a part of a clinician as well as a pathologist to know the pattern in which these hormones are secreted along with their physiological roles. Thus this chapter includes the disease that are related to excess as well as deficiencies of the hormones secreted by adrenal cortex. The chapter also includes various genetic syndromes that are associated with the disorders associated with hormones of adrenal cortex. The last part of the chapter includes a brief description of various benign as well as malignant lesions, the pathological as well as the etiological aspects and the hormonal abnormalities associated. This chapter thus mainly focuses on the pathology associated with the adrenal cortex and hormones secreted by the various layers of adrenal cortex.
Part of the book: Mitochondria and Brain Disorders
Mitochondria are major intracellular organelles with a variety of critical roles like adenosine triphosphate production, metabolic modulation, generation of reactive oxygen species, maintenance of intracellular calcium homeostasis, and the regulation of apoptosis. Mitochondria often undergo transformation in both physiological and pathological conditions. New concepts point that mitochondrial shape and structure are intimately linked with their function in the kidneys and diseases related to mitochondrial dysfunction have been identified. Diseases associated with mitochondrial dysfunction are termed as “mitochondrial cytopathies”. Evidence support that there is a role of mitochondrial dysfunction in the pathogenesis of two common pathways of end-stage kidney disease, namely, chronic kidney disease (CKD) and acute kidney injury (AKI). Mitochondrial cytopathies in kidneys mainly manifest as focal segmental glomerular sclerosis, tubular defects, and as cystic kidney diseases. The defects implicated are mutations in mtDNA and nDNA. The proximal tubular cells are relatively vulnerable to oxidative stress and are therefore apt to suffer from respiratory chain defects and manifest as either loss of electrolyte or low-molecular-weight proteins. Patients with mitochondrial tubulopathy are usually accompanied by myoclonic epilepsy and ragged red muscle fibers (MERRF), and Pearson’s, Kearns-Sayre, and Leigh syndromes. The majority of genetic mutations detected in these diseases are fragment deletions of mtDNA. Studies have shown significantly increased ROS production, upregulation of COX I and IV expressions, and inactivation of complex IV in peripheral blood mononuclear cells of patients with stage IV–V CKD, thereby demonstrating the close association between mitochondrial dysfunction and progression to CKD. Furthermore, the mechanisms that translate cellular cues and demands into mitochondrial remodeling and cellular damage, including the role of microRNAs and lncRNAs, are examined with the final goal of identifying mitochondrial targets to improve treatment of patients with chronic kidney diseases.
Part of the book: Mutagenesis and Mitochondrial-Associated Pathologies