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Patient complains of increasing anorexia and nausea coupled with weight gain, severe itchiness and muscle cramps. Processes that facilitate progression to end-stage kidney disease in the obese and diabetic patient are examined including deleterious effects of hyperglycemia, dysregulation of the renin–angiotensin–aldosterone system, oxidative damage, medullary hypoxia, progressive metabolic acidosis, and interglomerular hemodynamic and structural alterations. Published guidelines for managing the patient with chronic kidney disease are presented, with emphasis on current guidelines for protein and vitamin D intake. Evidence for targeted dietary strategies to optimize gut microbiota and modulate hyperglycemia and dyslipidemia are discussed, as well as strategies to optimize electrolyte levels and acid load, maintain bone integrity, and reduce risk for arterial calcification in the CKD patient. Special emphasis is placed on strategies to reduce the deleterious effects of high sodium and phosphorus intake on kidney injury, osteodystrophy, and calciphylaxis.

The disruption of multiorgan systems biology produced by renal injury in early stages of kidney injury and disease was unrecognized until its elucidation during the investigation of the chronic kidney disease-mineral bone disorder (CKD-MBD). The disordered systems biology causes the CKD-MBD and contributes to major components of increased cardiovascular risk for CKD patients. The result, in addition to the previously recognized renal osteodystrophy, is increased cardiovascular mortality in CKD. The inception of the CKD-MBD was only recently realized to begin with the early effects of kidney disease, and its pathophysiology involves circulating factors produced by renal repair and newly discovered hormones, such as FGF23 and cut klotho. Progressing from its inception, the disruption of the multiorgan system leads to the pathophysiology previously recognized as secondary hyperparathyroidism, hyperphosphatemia, calcitriol deficiency, and renal osteodystrophy that are now incorporated into the CKD-MBD syndrome.

Publisher Summary This chapter describes toxicity of chemicals that target the renal system. Toxicants and toxins can produce their effects on the different anatomical locations of the kidneys by affecting the tubules, glomeruli, ducts, vessels, and interstitium. The majority of toxins manifest their effects by acute renal failure. The most important manifestation of acute renal failure is the decrease in glomerular filtration rate (GFR) that leads to an excess of urea or other nonprotein nitrogenous components in the blood (azotemia). The decrease in GFR can be due to prerenal, renal, or postrenal causes. Renal toxicity generally leads to renal or sometimes postrenal azotemia. Postrenal azotemia is usually observed in conditions of obstruction to renal outflow or postrenal leakage. The toxic effects of chemicals on the kidneys result in reduced GFR, leading to azotemia. Clinical signs of chronic renal failure primarily include: edema due to reduced renal perfusion leading to stimulation of the renin–angiotensin system, which stimulates aldosterone secretion leading to retention of sodium and water, hypocalcemia with compensatory parathyroid activity, and osteodystrophy, and reduced red blood cell counts due to decreased synthesis of erythropoietin as a result of damage to the juxtaglomerular cells. Urine analysis is one of the most important methodologies to evaluate renal function and to interpret injury to the various anatomical components of the kidneys. Urine analysis involves multiple physical and chemical parameters as well as sediment analysis.

This chapter focuses on the role of bone biopsy in osteoporosis. The nondecalcified bone biopsy has been an invaluable tool in diagnosing and following treatment of numerous metabolic disorders of bone, the most significant example of which may be renal osteodystrophy. This family of skeletal disorders that accompanies renal failure is now remarkably well understood and largely treatable and preventable, the latter as a result of the availability of the nondecalcified bone biopsy. The histologic examination is the most effective means of documenting aluminum-induced osteodystrophy. The bone biopsy can often prove to be diagnostic in osteoporotic syndromes especially in patients with nonsecreting forms of multiple myeloma, and others with systemic mastocytosis. Patients with osteomalacia often remain misdiagnosed, because blood levels of 25-(OH)D 3 may prove misleading in this regard. The potential of the bone biopsy in treating the osteoporotic patient can be utilized in order to characterize the cellular aspects of the osteoporotic process.

Chronic renal failure means progressive and irreversible destruction of nephrons involving almost every organ system of the body. Early diagnosis of the disease and conservative therapy can slow down progression towards end stage renal disease. Nocturia/polyuria, anaemia, hypertension, osteodystrophy, reduced kidney size and associated acute renal failure are features which help physician in an early diagnosis. Detailed evaluation of these features has been suggested.

This chapter focuses on X-linked phenotypes. Agammaglobulinemia, Swiss type, is a type of disease that differs from the Bruton type by the presence of lymphocytosis, earlier age of death, vulnerability to viral, fungal, and bacterial infections, lack of delayed hypersensitivity, atrophy of the thymus, and lack of benefit by gamma globulin administration. Albright's hereditary osteodystrophy comprises both pseudohypoparathyroidism and pseudo-pseudohypoparathyroidism, which are probably aspects of a single entity. The manifestations of Aldrich syndrome are eczema, thrombocytopenia, proneness to infection, and bloody diarrhea. Death occurs before age 10. Aldrich's original kindred was of Dutch extraction. In amelogenesis imperfecta, hypoplastic type—hereditary enamel hypoplasia—the enamel is very hard but is abnormally thin so that the teeth appear small. The surface is rough. This type is inherited as an X-linked dominant. Possible genetic relationship, for example, allelism, with the factor for the hypomaturation type is unknown. Therefore, the two have been listed as separate loci.