142 Summary of Recommendation Statements 143 Chapter 1: Introduction 154 Chapter 2: General principles in the management of glomerular disease 156 Chapter 3: Steroid-sensitive nephrotic syndrome in children 163 Chapter 4: Steroid-resistant nephrotic syndrome in children 172 Chapter 5: Minimal-change disease in adults 177 Chapter 6: Idiopathic focal segmental glomerulosclerosis in adults 181 Chapter 7: Idiopathic membranous nephropathy 186 Chapter 8: Idiopathic membranoproliferative glomerulonephritis 198 Chapter 9: Infection-related glomerulonephritis 200 Chapter 10: Immunoglobulin A nephropathy 209 Chapter 11: Henoch-Schönlein purpura nephritis 218 Chapter 12: Lupus nephritis 221 Chapter 13: Pauci-immune focal and segmental necrotizing glomerulonephritis 233 Chapter 14: Anti-glomerular basement membrane antibody glomerulonephritis 240 Methods for guideline development 243 Biographic and Disclosure Information 252

KDIGO Clinical Practice Guideline for Glomerulonephritis

Solid-organ transplantation is a therapeutic option for many human diseases. Infections are a major complication of solid-organ transplantation. All candidates should undergo a thorough infectious-disease screening prior to transplantation. There are three time frames, influenced by surgical factors, the level of immunosuppression, and environmental exposures, during which infections of specific types most frequently occur posttransplantation. Most infections during the first month are related to surgical complications. Opportunistic infections typically occur from the second to the sixth month. During the late posttransplant period (beyond 6 months), transplantation recipients suffer from the same infections seen in the general community. Opportunistic bacterial infections seen in transplant recipients include those caused by Legionella spp., Nocardia spp., Salmonella spp., and Listeria monocytogenes. Cytomegalovirus is the most common cause of viral infections. Herpes simplex virus, varicella-zoster virus, Epstein-Barr virus and others are also significant pathogens. Fungal infections, caused by both yeasts and mycelial fungi, are associated with the highest mortality rates. Mycobacterial, pneumocystis, and parasitic diseases may also occur.

Infections in solid-organ transplant recipients.

Background Defining the most appropriate treatment for patients with idiopathic membranous nephropathy is a matter of controversy. The course of the disorder is often benign, and the immunosuppressive regimens used in some patients have uncertain benefits and substantial risks. We studied the natural history of idiopathic membranous nephropathy in patients who received only symptomatic therapy. Methods We prospectively studied 100 consecutive patients (68 men and 32 women; mean [±SD] age, 51 ±17 years) with biopsy-proved idiopathic membranous nephropathy. The patients received diuretic or antihypertensive drugs as needed, but no glucocorticoid or immunosuppressive drugs. We examined the patients and measured their urinary protein excretion and serum creatinine concentrations every 6 months for a mean of 52 months. Results Twenty-four (65 percent) of the 37 patients followed for at least five years had complete or partial remission of proteinuria; in 6 others (16 percent), end-stage renal disease developed...

Prognosis of Untreated Patients with Idiopathic Membranous Nephropathy

) - ((HCO 3 - ) + (Cl - )), aids diagnosis by classifying the disorders into categories of normal (hyperchloremic) anion gap or elevated anion gap. These categories can overlap, however. Adverse effects of acute metabolic acidosis primarily include decreased cardiac output, arterial dilatation with hypotension, altered oxygen delivery, decreased ATP production, predisposition to arrhythmias, and impairment of the immune response. The main adverse effects of chronic metabolic acidosis are increased muscle degradation and abnormal bone metabolism. Using base to treat acute metabolic acidosis is controversial because of a lack of definitive benefit and because of potential complications. By contrast, the administration of base for the treatment of chronic metabolic acidosis is associated with improved cellular function and few complications.

/pdf/metabolic-acidosis-pathophysiology-diagnosis-and-management-51e9gfqqps.pdf

Metabolic acidosis: pathophysiology, diagnosis and management

Hepatitis B infection and renal disease: clinical, immunopathogenetic and therapeutic considerations.

The Urine Anion Gap: A Clinically Useful Index of Ammonium Excretion

Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis.

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease

A controlled trial of cyclophosphamide in patients with membranous glomerulonephritis

A 21-year old woman with poorly controlled diabetes mellitus was examined for persistent hyperchloremic metabolic acidosis. There was no evidence of ingestion of hydrochloric acid or its equivalent. Gastrointestinal loss of bicarbonate was absent. Proximal tubular bicarbonate reabsorption and distal nephron hydrogen-ion secretion were normal. Ammonia and net acid excretions were high, and thus there was no obvious cause for this acidosis. Further study revealed a very large loss of β-hydroxy-butyrate in the urine that closely approximated net acid excretion. This loss of potential bicarbonate was the principal cause for the hyperchloremic metabolic acidosis. Phosphate, urate, and β-hydroxybutyrate fractional excretions were all abnormally high. Generalized aminoaciduria was also present, but the renal handling of glucose and bicarbonate was normal. With improved control of her diabetes, the generalized aminoaciduria disappeared, the urine β-hydroxybutyrate loss ceased, the fractional excretions of phosphate and urate approached normal, and the acidosis was rapidly corrected.

Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of pathophysiologic mechanisms.

The urine osmolal gap is defined as the difference between measured urine osmolality and the sum of the concentrations of sodium, potassium, chloride, bicarbonate, urea and glucose. Normally, this gap is 80-100 mosmol/kg H2O. A determination of the urine osmolal gap may be useful to ascertain the etiology of metabolic acidosis which is of the mixed wide and normal plasma anion gap type ("hybrid" metabolic acidosis). For example, with "hybrid" metabolic acidosis, a low urine osmolal gap will suggest the absence of excessive organic aciduria (ketoacidosis) and the basis of the normal anion gap type of acidosis will be determined by the urine anion gap or "net charge". Where "hybrid" metabolic acidosis has occurred due to wide anion gap metabolic acidosis with loss of organic acid anion in the urine, the urine osmolal gap will be high and can be used in a semi-quantitative fashion to estimate the sum of urinary ammonium plus ketone body anion concentrations.

Robert A. Bear

Papers

The Urine Anion Gap: A Clinically Useful Index of Ammonium Excretion

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease

A controlled trial of cyclophosphamide in patients with membranous glomerulonephritis

Hyperchloremic metabolic acidosis in diabetes mellitus: a case report and discussion of pathophysiologic mechanisms.

The urine osmolal gap: a clue to estimate urine ammonium in "hybrid" types of metabolic acidosis.