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The most common cause of kidney failure in the United States and across the world is diabetes mellitus (DM). Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in persons with diabetes, and chronic kidney disease (CKD) further increases overall CVD risk. It is important to individualize glycemic targets for patients to maintain glucose levels that will reduce the development and progression of complications while avoiding hypoglycemia. CKD alters the relationship of glucose levels to measures of long-term control, such as hemoglobin A 1c . Medications used to treat DM may need dose adjustments as CKD progresses. Some medications have particular characteristics in patients with CKD. Insulin and sulfonylureas increase the risk of hypoglycemia, some glucagon-like peptide 1 receptor agonists reduce the risk of CVD outcomes, and most sodium/glucose cotransporter 2 inhibitors reduce the risk of CKD and CVD outcomes. Therefore, for the individual patient, changes in medication types and doses may need constant attention as CKD progresses., (Copyright © 2021 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Prolactin levels are increased in chronic kidney disease (CKD) as a result of reduced clearance and increased secretion. Hyperprolactinemia manifests as galactorrhea and hypogonadism. Treatment of hyperprolactinemia should focus on improving bothersome galactorrhea or hypogonadism by using dopamine agonists and/or replacement of sex hormone(s). Changes in the hypothalamic-pituitary-adrenal axis in CKD are characterized by increases in adrenocorticotropic hormone (ACTH) and cortisol levels, largely preserved circadian rhythms of ACTH and cortisol, and a normal response of cortisol to ACTH, metyrapone, and insulin-induced hypoglycemia. However, the hypothalamic-pituitary-adrenal axis is less inhibited by 1 mg dexamethasone but retains normal suppression by higher-dose dexamethasone. Diagnosis of adrenal insufficiency in CKD patients, as in normal subjects, usually is made by finding a subnormal cortisol response to ACTH. The mainstay of treatment of adrenal insufficiency is to replace glucocorticoid hormone. Cushing's disease in CKD is difficult to diagnose and relies on the dexamethasone suppression test and the midnight salivary cortisol test because the 24-hour urine free cortisol test is not useful because it is increased already in CKD. Treatment of Cushing's disease involves surgery, complemented by radiation and/or medical therapy if necessary. Growth hormone levels are increased and insulin-like growth factor 1 levels are normal in patients with CKD. In a normal patient with CKD, as in one with acromegaly, there can be a paradoxic increase in growth hormone after an oral glucose load. Therefore, diagnosis of acromegaly in renal insufficiency is challenging. The treatment of choice for acromegaly is surgery, although data for medical treatment for acromegaly in CKD are rare. In patients with renal impairment, arginine vasopressin levels are increased as a result of decreased clearance, and there also is impairment of arginine vasopressin signaling in renal tubules. Diabetes insipidus can be masked in advanced kidney disease until kidney transplantation. Diagnosis of the syndrome of inappropriate antidiuretic hormone is similar in mild or moderate kidney disease as in normal subjects, but is challenging in patients with advanced kidney disease owing to the impairment in urine dilution., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Diabetes is the most frequent cause of chronic kidney disease (CKD), leading to nearly half of all cases of kidney failure requiring replacement therapy. The principal cause of death among patients with diabetes and CKD is cardiovascular disease (CVD). Sodium/glucose cotransporter 2 (SGLT2) inhibitors were developed to lower blood glucose levels by inhibiting glucose reabsorption in the proximal tubule. In clinical trials designed to demonstrate the CVD safety of SGLT2 inhibitors in type 2 diabetes mellitus (T2DM), consistent reductions in risks for secondary kidney disease end points (albuminuria and a composite of serum creatinine doubling or 40% estimated glomerular filtration rate decline, kidney failure, or death), along with reductions in CVD events, were observed. In patients with CKD, the kidney and CVD benefits of canagliflozin were established by the CREDENCE (Canagliflozin and Renal Events in Diabetes With Established Nephropathy Clinical Evaluation) trial in patients with T2DM, urinary albumin-creatinine ratio>300mg/g, and estimated glomerular filtration rate of 30 to<90mL/min/1.73m 2 . To clarify and support the role of SGLT2 inhibitors for treatment of T2DM and CKD, the National Kidney Foundation convened a scientific workshop with an international panel of more than 80 experts. They discussed the current state of knowledge and unanswered questions to propose therapeutic approaches and delineate future research. SGLT2 inhibitors improve glomerular hemodynamic function and are thought to ameliorate other local and systemic mechanisms involved in the pathogenesis of CKD and CVD. SGLT2 inhibitors should be used when possible by people with T2DM to reduce risks for CKD and CVD in alignment with the clinical trial entry criteria. Important risks of SGLT2 inhibitors include euglycemic ketoacidosis, genital mycotic infections, and volume depletion. Careful consideration should be given to the balance of benefits and harms of SGLT2 inhibitors and risk mitigation strategies. Effective implementation strategies are needed to achieve widespread use of these life-saving medications., (Copyright © 2020 The National Kidney Foundation, Inc and American Diabetes Association. Published by Elsevier Inc. All rights reserved.)

The incidence and prevalence of diabetes mellitus have grown significantly throughout the world, due primarily to the increase in type 2 diabetes. This overall increase in the number of people with diabetes has had a major impact on development of diabetic kidney disease (DKD), one of the most frequent complications of both types of diabetes. DKD is the leading cause of end-stage renal disease (ESRD), accounting for approximately 50% of cases in the developed world. Although incidence rates for ESRD attributable to DKD have recently stabilized, these rates continue to rise in high-risk groups such as middle-aged African Americans, Native Americans, and Hispanics. The costs of care for people with DKD are extraordinarily high. In the Medicare population alone, DKD-related expenditures among this mostly older group were nearly $25 billion in 2011. Due to the high human and societal costs, the Consensus Conference on Chronic Kidney Disease and Diabetes was convened by the American Diabetes Association in collaboration with the American Society of Nephrology and the National Kidney Foundation to appraise issues regarding patient management, highlighting current practices and new directions. Major topic areas in DKD included (1) identification and monitoring, (2) cardiovascular disease and management of dyslipidemia, (3) hypertension and use of renin-angiotensin-aldosterone system blockade and mineralocorticoid receptor blockade, (4) glycemia measurement, hypoglycemia, and drug therapies, (5) nutrition and general care in advanced-stage chronic kidney disease, (6) children and adolescents, and (7) multidisciplinary approaches and medical home models for health care delivery. This current state summary and research recommendations are designed to guide advances in care and the generation of new knowledge that will meaningfully improve life for people with DKD., (Copyright © 2014 American Diabetes Association and the National Kidney Foundation. Published by Elsevier Inc. All rights reserved.)

Clinically nonfunctioning pituitary adenomas range from those causing significant hypothalamic/pituitary dysfunction and visual field compromise to those being completely asymptomatic, detected either at autopsy or as incidental findings on imaging scans performed for other reasons (often referred to as pituitary incidentalomas). Growth of nonfunctioning pituitary adenomas without treatment occurs in about 10% of microadenomas and 24% of macroadenomas. In the absence of hypersecretion, hypopituitarism, or visual-field defects, periodic screening by magnetic resonance imaging may detect enlargement. Potential indications for surgery are growth of a pituitary incidentaloma, the development of visual-field defects, or the development of hypopituitarism., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Pituitary adenomas are the most common pituitary disorder affecting pregnancy, and prolactinomas are the most common of the hormone-secreting pituitary adenomas. Hyperprolactinemia must be corrected to allow ovulation and fertility. Bromocriptine has been shown to be safe for use during early gestation. There is less than a 2% risk of microprolactinoma enlargement during pregnancy but a greater than 15% risk of symptomatic enlargement of a macroprolactinoma. Treatment options for patients with macroadenomas include stopping bromocriptine when pregnancy is diagnosed and reinstituting with tumor enlargement, continuous bromocriptine throughout pregnancy, and prepregnancy tumor debulking by surgery. The diagnosis of acromegaly may be difficult to make during pregnancy and relies, in part, on the persistence of the normal pulsatile secretion of growth hormone and loss of this secretory characteristic with a tumor. The growth hormone oversecretion may exacerbate tendencies to gestational diabetes, fluid retention, and hypertension. Treatment for acromegaly and other tumors generally may be deferred until after delivery. There are rare reports of enlargement of clinically nonfunctioning and growth hormone secreting tumors during pregnancy, and surveillance is needed. Tumors may need to be differentiated from lymphocytic hypophysitis. Patients with chronic hypopituitarism usually will need treatment with gonadotropins or pulsatile GnRH to become pregnant and may need increased steroid coverage during labor and delivery. Hypopituitarism developing during pregnancy is usually caused by lymphocytic hypophysitis and usually also will require steroid replacement therapy. Hypopituitarism arising postpartum may be caused by either lymphocytic hypophysitis or Sheehan's syndrome, and the latter may present as an acute or chronic syndrome. Borderline diabetes insipidus may manifest during pregnancy because of increased vasopressin degradation caused by markedly increased levels of placental vasopressinase. Treatment with desmopressin usually is satisfactory. Patients presenting with either anterior or posterior pituitary insufficiency in the peripartum period should always be evaluated for function of the other portion of the pituitary.

Diabetic nephropathy is a major cause of morbidity and mortality in patients with diabetes and occurs in about one-third of such patients. The course of nephropathy has become better defined, with patients initially developing microalbuminuria (albumin excretion rates [AER] between 20 and 200 micrograms/min), then overt nephropathy (AER > or = 200 micrograms/min) and finally a decline in GFR eventuating in end-stage renal disease (ESRD). Although metabolic control has long been hypothesized as a contributor to the development of nephropathy, it is only in recent years that this hypothesis has been proven. A number of observational studies have shown correlations between glycemic control and the development of various levels of albuminuria and also declines in GFR. Several small, prospective, randomized, interventional studies and the Diabetes Control and Complications Trial (DCCT) have now definitely proven that improved metabolic control that achieves near-normoglycemia can significantly decrease the development and progression of early nephropathy as well as other long-term complications of diabetes, including retinopathy and neuropathy. It is now conceivable that the achievement of near-normoglycemia plus the addition of angiotensin-converting enzyme inhibitors if microalbuminuria develops may greatly decrease the numbers of patients eventually requiring renal replacement therapy.

The case of a 58-year-old man with nephrotic syndrome and characteristic pathologic renal lesions of KW disease is presented. No evidence of diabetes was found by oral or intravenous glucose tolerance tests. The possibilities of light-chain disease, membranoproliferative form of glomerulonephritis, and amyloidosis were excluded by histochemistry and immunofluorescent microscopy.

Hyperprolactinemia is common in patients with renal failure. Because radiographic contrast material given during a computed tomographic (CT) scan of the sella as part of the evaluation for prolactinoma worsens renal insufficiency, we attempted to define the point at which hyperprolactinemia becomes an expected finding in patients with renal insufficiency in this study. Of 59 patients with serum creatinine levels of 1.5 to 12 mg/dL, 16 (27.1%) were hyperprolactinemic. Of these 16, nine were not taking medications known to raise prolactin levels and their prolactin levels were less than 100 ng/mL. In the eight patients taking medications prolactin levels were much higher. In one patient the prolactin level fell from 2,210 to 100 ng/mL when methyldopa was discontinued. In patients with chronic renal failure prolactin levels were similar regardless of the method of dialysis. We conclude that in the absence of medications known to affect prolactin secretion, hyperprolactinemia occurs infrequently (18.3%) and, when it occurs, is mild (less than 100 ng/mL). Marked hyperprolactinemia may occur in patients taking such medications. These should be stopped and the prolactin level rechecked before a CT scan is performed.

Depressed triiodothyronine and elevated reverse triiodothyronine levels are commonly seen in patients with acute and chronic illness and in patients receiving markedly hypocaloric diets. To investigate the role of nutritional adequacy in causing the altered thyroid hormone levels found in severe illness, we studied patients with bacterial sepsis who were receiving a variety of nutritional regimens. Thirteen patients received only 5% dextrose in water (600-1000 kcal/day), 7 of whom were in shock. Seven patients received total parenteral nutrition (2500-3500 kcal/day). Analysis of thyroid hormone levels in these groups and in controls shows that a large component of the alteration in thyroid hormone levels found in patients with severe illness is due to the caloric deprivation associated with such severe illness.