Diuretics are important clinical tools used for the treatment of hypervolemic states and hypertension. Classes of diuretics are defined by either the location within the nephron at which inhibition occurs or their mechanism of action and include carbonic anhydrase inhibitors, sodium-glucose transporter inhibitors, thiazides, loop diuretics, epithelial sodium channel inhibitors, mineralocorticoid antagonists, osmotic diuretics, and vasopressin receptor antagonists. An understanding of normal kidney sodium balance is necessary to ensure adequate dosing parameters. Therapeutic indications, dosage nuances, concurrent chronic disease processes and adverse effects often dictate which class of diuretic is initially utilized. Diuretic resistance has resulted in adaptation of the treatment paradigm and often requires combination therapy for resolution. Isolated ultrafiltration devices have been evaluated but require further investigation prior to widespread use.

IgA nephropathy (IgAN) is the most common pattern of glomerulonephritis in much of the world and remains an important cause of chronic kidney disease and kidney failure. Much progress has been made in our understanding of the genetic and biochemical pathogenic basis of the disease. The Oxford Classification, a histopathology scoring system developed for IgAN in 2009, is widely validated and adopted. Current treatment of IgAN remains generic to many chronic kidney diseases and glomerulonephritides, while optimal treatment strategies and emerging therapeutic approaches are continually being developed and tested in clinical trials. IgA vasculitis (or Henoch-Schönlein purpura) is a systemic form of vasculitis involving the kidney, gut, skin, and joints but shares many distinct clinical features with IgAN in its kidney involvement.

Minimal change disease (MCD) is a common cause of nephrotic syndrome (NS). Although MCD is defined by minor changes on light microscopy and the presence of foot process effacement on electron microscopy, it can be diagnosed clinically by exhibiting responsiveness to corticosteroid treatment. In children, MCD is the cause of up to 90% of cases of idiopathic NS in contrast to adults where it is observed in 10%-15% of patients with new-onset disease. The pathogenesis of MCD is not well understood, but likely represents a variable interaction between intrinsic glomerular podocyte defects and immunologic disturbances. MCD presents with nephrotic-range proteinuria, edema, hypoalbuminemia, and hypercholesterolemia. A hypercoagulable state secondary to the NS is much more common in adult versus pediatric patients. Corticosteroids represent the time-honored initial therapy for presumed and biopsy-confirmed MCD and are effective in 60%-90% of patients depending on age. Second-line immunosuppressive therapy, including calcineurin inhibitors, mycophenolate mofetil, and rituximab, is used in patients with frequently relapsing and steroid-dependent MCD, as well as those who experience, or are at risk from, steroid-related side effects. Recent interventional trials aim to improve clinical and patient-reported outcomes in patients with MCD. Supportive care involves diet and diuretics to control edema, use of lipid-lowering drugs, and immunizations to prevent infection. The long-term prognosis of MCD is excellent with eventual resolution of the disease without any permanent kidney injury. Future research is needed to better define the cause of MCD with the development of more targeted treatments that can effectively achieve long-term remission without the side effects associated with current therapeutic options.

In this chapter, the evaluation and selection of appropriate kidney transplant recipients and living kidney donors are reviewed. For recipient selection, important issues in the medical evaluation, such as age, obesity, cause of end-stage kidney disease, cancer, and cardiovascular disease, among others, are reviewed. Relative contraindications and appropriate tests to be performed prior to transplantation are discussed. For living donor selection, key aspects of the informed consent process, medical evaluation, and psychosocial assessment are reviewed. The evaluation of deceased-donor kidney quality and principles of allocation are also reviewed.

Kidney involvement in systemic lupus erythematosus, termed lupus nephritis (LN), occurs in 50% to 75% of lupus patients and is a significant cause of lupus-associated morbidity and mortality, including end-stage kidney disease. LN is a paradigm of immune complex–mediated kidney injury: The immune deposits that incite LN are primarily complexes of anti-double-stranded DNA antibodies directed against nucleosomal antigens. However, the pathogenesis is complex, involving abnormalities in multiple components of the immune system, including B and T cells, the complement cascade, cytokines, and clearance of apoptosis. The diagnosis of LN is suspected by changes in laboratory parameters—elevated serum creatinine, presence of hematuria and/or proteinuria, low serum complement levels—but still hinges on the kidney biopsy with glomerular changes being the major determinant of classification. The current approach to treating LN is guided by histologic findings (i.e., International Society of Nephrology (ISN)/Renal Pathology Society (RPS) class and the degree of activity and chronicity), with appropriate consideration of presenting clinical parameters and the degree of kidney function impairment. Treatment regimens for LN typically utilize combination therapy of corticosteroids with cyclophosphamide or mycophenolate. After remission is obtained, maintenance therapy involves a tapering dose of corticosteroids combined with an antimetabolite. LN has been shown to impact clinical outcomes in systemic lupus erythematosus (SLE) both directly via target organ damage and indirectly through complications of therapy.