Nephrology: An Annotated Bibliography of Recent Literature
Authors: NEPHROLOGY COMMITTEE
Journal: Annals of Internal Medicine (1976)

The Literature of Medicine1 January 1976Nephrology: An Annotated Bibliography of Recent LiteratureReferences to Journal Articles and Other PapersNEPHROLOGY COMMITTEENEPHROLOGY COMMITTEESearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-84-1-104 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThis bibliography includes references to 99 recently published journal papers and similar sources that represent recent developments important in the concepts and practice of internal medicine. In has been compiled as a part of the work of the Nephrology Committee toward the preparation of the Medical Knowledge Self-Assessment Program IV Syllabus.In preparing this bibliography, the committee reviewed MEDLINE†bibliographic printouts of journal articles published since the beginning of 1972 and also drew on their own files. Papers were selected with a view to their likely availability in libraries of hospitals and other clinical institutions in the United States and...Sodium, Water, and Potassium Metabolism Acid-Base Disturbances Calcium, Phosphorus, and Magnesium Metabolism Hypertension and the Kidney Glomerular and Interstitial Renal Diseases Obstructive Nephropathy Acute Renal Failure Chronic Renal Failure Dialysis Renal Transplantation1. MOSESMILLER AM: Drug-induced hyponatremia. N Engl J Med 291:1234-1238, 1974 A good review of how drugs interfere with renal water excretion, thereby producing clinical hyponatremia. CrossrefMedlineGoogle Scholar2. SCHRIERBERL RT: Non-osmolar factors affecting renal water excretion. N Engl J Med 292:81-88; 141-146, 1975 The best new review on volume receptors, hormones, neural stimuli, and other nonosmolar factors affecting renal water excretion. CrossrefMedlineGoogle Scholar3. GOLDBERG M: Water control and the dysnatremias, in The Sea Within Us, edited by BRICKER NS, SELDIN DW. New York, Plenum Publishing Corp., 1975, pp. 14-25 A good new review that stresses the relation between body fluid volume and the concentration distribution of osmotically active solute in cells and extracellular compartments. A good approach to clinical states of hypertonicity and hypotonicity. Google Scholar4. ALFORDSCOGGINSWHARTON FBC: Symptomatic normovolemic essential hypernatremia. Am J Med 54:359-370, 1973 A case report that presents convincing evidence for abnormal hypothalamic osmoreceptor function resulting in persistent hypernatremia. The pathogenesis of the defect in this patient was unclear. There was no demonstrable central nervous system lesion. CrossrefMedlineGoogle Scholar5. HARRINGTONCOHEN JJ: Clinical disorders of urine concentration and dilution. Arch Intern Med 131:810-825, 1973 A reasonable clinical guide to the differential diagnosis and management of the relatively common clinical disorders of urinary concentrating and diluting defects. CrossrefMedlineGoogle Scholar6. DOUSA T: Cellular action of antidiuretic hormone in nephrogenic diabetes insipidus. Proc Mayo Clin 49:188-199, 1974 More specific information of mechanisms involved in normal water metabolism and clinical defects in renal water conservation. MedlineGoogle Scholar7. KLAHRSLATOPOLSKY SE: Renal regulation of sodium excretion. Arch Intern Med 131:780-791, 1973 A basic, general review of those factors that determine renal sodium excretion and extracellular fluid volume, emphasizing different function by different segments of the nephron and how they are affected in edema states. CrossrefMedlineGoogle Scholar8. MARTINEZ-MALDONADOEKNOYANSUKI MGW: Diuretics in nonedematous states. Arch Intern Med 131:797-808, 1973 A very interesting way of looking at diuretic drugs and the new ways in which this group of agents can be used to treat, for example, abnormalities of calcium metabolism or renal stone formation. CrossrefMedlineGoogle Scholar9. SCHULTZE R: Recent advances in the physiology and pathophysiology of potassium excretion. Arch Intern Med 131:885-897, 1973 The best recent review, which covers not only the normal metabolism of this ion but newer states of abnormal potassium regulation. CrossrefMedlineGoogle Scholar10. MICHELISMURDAUGH MH: Selective hypoaldosteronism. Am J Med 59:1-5, 1975 This paper reviews all previously reported cases of this now commonly recognized and important syndrome. CrossrefMedlineGoogle Scholar11. FELIG P: Diabetic ketoacidosis. N Engl J Med 290:1360-1363, 1974 An excellent, brief review of modern concepts of pathogenesis and treatment of diabetic ketoacidosis. CrossrefMedlineGoogle Scholar12. COOPERMANDAVIDOFFSPARK MFR: Clinical studies of alcoholic ketoacidosis. Diabetes 23:433-439, 1974 Alcoholic ingestion can result in marked ketoacidosis without hyperglycemia or glycosuria. CrossrefMedlineGoogle Scholar13. HEIRDDELLDRISCOLL WRJ: Metabolic acidosis resulting from intravenous alimentation mixtures containing synthetic amino acids. N Engl J Med 287:943-948, 1972 Total parenteral nutrition using synthetic L-amino acids as a source of nitrogen may result in metabolic acidosis due to generation of a net excess of hydrogen ions from the cationic anion acids in some preparations. CrossrefMedlineGoogle Scholar14. RASTEGARTHIER AS: Physiologic consequences and bodily adaptations to hypercapnia and hypocapnia. Chest 62(suppl):28S-34S, 1972 This review summarizes the nature and extent of the normal physiologic responses to primary acid-base disturbances of respiratory origin. Emphasizes the importance of distinguishing between acute and chronic disturbances. CrossrefGoogle Scholar15. MCCURDY D: Mixed metabolic and respiratory acid-base disturbances: diagnosis and treatment. Chest 62(suppl):35S-44S, 1972 This unusually readable review summarizes the nature and extent of the normal physiologic responses to primary metabolic acid-base disturbances. In addition, the author reviews the diagnosis and treatment of the common "mixed" disturbances. CrossrefGoogle Scholar16. KASSIRER J: Serious acid-base disorders. N Engl J Med 291:773-776, 1974 This brief review provides a capsule summary of the major diagnostic and therapeutic considerations that arise in the management of life-threatening acid-base disorders. CrossrefMedlineGoogle Scholar17. GARELLADANACHAZAN SCJ: Severity of metabolic acidosis as a determinant of bicarbonate requirements. N Engl J Med 289:121-126, 1973 Extreme reductions in plasma bicarbonate concentration (less than 4 meq/litre) may signify the need for disproportionate amounts of bicarbonate replacement therapy. CrossrefMedlineGoogle Scholar18. MAZZARAAYRESGRACE JSW: Extreme hypocapnia in the critically ill patient. Am J Med 56:450-456, 1974 Arterial PCO2 was frequently found to be decreased in this large series of critically ill patients and was highly correlated with survival, extreme reductions auguring poorly. The pathogenesis, differential diagnosis, and treatment of hypocapnia are discussed. CrossrefMedlineGoogle Scholar19. ABERMANFULOP AM: The metabolic respiratory acidosis of acute pulmonary edema. Ann Intern Med 76:173-184, 1972 In a large group of patients with pulmonary edema, a wide-range of arterial PCO2 was found; significant hypercapnia was not uncommon. An element of metabolic acidosis was also frequently detected, especially in patients with hypercapnia. LinkGoogle Scholar20. MAKOFF D: Acid-base metabolism, in Clinical Disorders of Fluid and Electrolyte Metabolism, 2nd ed., edited by MAXWELL MH, KLEEMAN CR. New York, McGraw-Hill Book Co., 1972, pp. 297-346 This well-written chapter can serve as an excellent "refresher" course in modern concepts of acid-base physiology; it provides a thorough background for more in-depth reading about clinical acid-base disturbances (229 references). Google Scholar21. SELDINRECTOR DF: The generation and maintenance of metabolic alkalosis. Kidney Int 1:306-321, 1972 Provides a thorough review of the pathophysiology and clinical features of metabolic alkalosis. The issue in which this paper appears was devoted to acid-base metabolism and contains many other useful monographs. CrossrefMedlineGoogle Scholar22. REISS E: Hyperparathyroidism—current perspectives. Adv Intern Med 19:287-301, 1974 A review of the chemistry, secretion, and metabolism of parathyroid hormone (PTH), which explains conflicting results from PTH immunoassay. The natural history of hyperparathyroidism and pre-operative localization of adenomas by venous catheterization are reviewed. MedlineGoogle Scholar23. DEFTOSNEER LR: Medical management of the hypercalcemia of malignancy. Ann Rev Med 25:323-331, 1974 Bone destruction by tumor, production of a parathyroidlike substance, a vitamin D sterol, or local prostaglandins may mediate such hypercalcemia. Hydration, calciuretic diuretics, sodium sulfate, inorganic phosphate, mithramycin, calcitonin, and glucocorticoids have therapeutic indications. CrossrefMedlineGoogle Scholar24. SCHNEIDERSHERWOOD AL: Pathogenesis and management of hypoparathyroidism and other hypocalcemia disorders. Metabolism 24:871-898, 1975 Reviews the factors responsible for maintaining normal serum calcium (for example, parathyroid hormone, vitamin D, and, perhaps, calcitonin); the signs, symptoms, and causes of hypocalcemia; and both acute and long-term management of hypocalcemia. CrossrefMedlineGoogle Scholar25. RODRIQUEZVILLARREALKLAHR HHS: Pseudohypoparathyroidism type II: restoration of normal renal responsiveness to parathyroid hormone by calcium administration. J Clin Endocrinol Metab 39:693-701, 1974 This form of pseudohypoparathyroidism is not due to failure of generation of cyclic AMP in response to parathyroid hormone, as is usual, but presumably to lack of cellular response to the cyclic AMP generated. CrossrefMedlineGoogle Scholar26. SUHTASHJIANMATSUO SAN: Pathogenesis of hypocalcemia in primary hypomagnesemia: normal end-organ responsiveness to parathyroid hormone, impaired parathyroid gland function. J Clin Invest 52:153-160, 1973 This case study points out, as do subsequent reports, that the hypocalcemia which commonly accompanies magnesium depletion may arise because of failure of the parathyroid glands to secrete PTH normally. CrossrefMedlineGoogle Scholar27. ALFREYMILLERBUTKUS AND: Evaluation of body magnesium stores. J Lab Clin Med 84:153-162, 1974 Muscle magnesium varied directly with muscle potassium rather than serum magnesium; serum magnesium correlated with bone magnesium. The magnesium pool in bone and extracellular fluid is labile and varies during magnesium surfeit or deficit; muscle magnesium may not reflect body magnesium stores. MedlineGoogle Scholar28. COBURNHARTENBOWERNORMAN JDA: Metabolism and action of the hormone vitamin D and its relation to calcium homeostasis. West J Med 121:22-44, 1974 Data on vitamin D conversion to 1,25 dihydroxy-vitamin D3 (1,25(OH)2D3), its mechanism of action, and disorders that may involve altered vitamin D action (that is, cirrhosis, anticonvulsant therapy, uremia, hypoparathyroidism, sarcoidosis, and idiopathic hypercalciuria) are reviewed. MedlineGoogle Scholar29. DELUCA H: The kidney as an endocrine organ involved in the function of vitamin D. Am J Med 58:39-47, 1975 Reviews the metabolic conversion of vitamin D to 1,25 dihydroxy-vitamin D3, and the factors that stimulate production of 1,25(OH)3D3 in kidneys of experimental animals (low calcium diet, parathyroid hormone, and lowered serum or tissue phosphate). CrossrefMedlineGoogle Scholar30. DAVID D: Calcium metabolism in renal failure. Am J Med 58:48-56, 1975 A current view of the pathogenic factors leading to renal osteodystrophy and altered calcium metabolism in uremia; current therapeutic approaches. CrossrefMedlineGoogle Scholar31. MASSRYBLUESTONEKLINENBERG SRJ: Abnormalities of the musculoskeletal system in hemodialysis patients. Semin Arthritis Rheum 4:321-349, 1975 The rheumatic syndromes, pyogenic skeletal infections, and ischemic subchondral necrosis of subchondral bone are reviewed. The features of soft tissue calcifications, the syndrome characterized by skin ulceration and tissue necrosis (calciphylaxis), and azotemic bone disease are also discussed. CrossrefMedlineGoogle Scholar32. TATLERBAILLODVARGHESE GRZ: Evolution of bone disease over 10 years in 135 patients with terminal renal failure. Br Med J 4:315-319, 1973 A progressively increasing incidence of secondary hyperparathyroidism occurred with the duration of dialysis, despite use of adequate dialysate calcium and prevention of hyperphosphatemia. A role of other, poorly understood factors is suggested. CrossrefMedlineGoogle Scholar33. BRICKMANSHERRARDJOWSEY ADJ: 1,25-dihydroxycholecalciferol. Effect on skeletal lesions and plasma parathyroid hormone levels in uremic osteodystrophy. Arch Intern Med 134:883-888, 1974 Plasma parathyroid hormone fell and excessive bone resorption improved after administration of 1,25(OH)2D3 to uremic patients. The potency of 1,25(OH)2D3 in uremia underscores a role of altered vitamin D metabolism in pathogenesis of renal osteodystrophy. CrossrefMedlineGoogle Scholar34. MASSRYFRIEDLERCOBURN SRJ: The physiology of the renal excretion of phosphate and calcium and its relation to clinical medicine. Arch Intern Med 131:828-859, 1973 The renal handling of calcium and phosphorus, the effects of hormonal and nonhormonal factors, and the influence of various disease states are reviewed. Uses of diuretics for hypercalciuria (thiazides) or hypercalcemia (furosemide) are presented. CrossrefMedlineGoogle Scholar35. COEKAVALACH FA: Hyperuricemia and hyperuricosuria in patients with calcium nephrolithiasis. N Engl J Med 291:1344-1350, 1974 Idiopathic hypercalciuria and stones may arise because of reduced tubular calcium reabsorption or because of increased intestinal absorption. With increased serum or urinary uric acid, thiazides or allopurinol can reduce the incidence of stones. CrossrefMedlineGoogle Scholar36. PAKOHATALAWRENCE CME: The hypercalciurias: causes, parathyroid functions and diagnostic criteria. J Clin Invest 54:387-400, 1974 An evaluation of parathyroid function and calcium metabolism in hypercalciuria. In hyperparathyroidism, hypercalciuria results largely from skeletal resorption; idiopathic hypercalciuria was due to excess intestinal absorption or impaired tubular reabsorption of calcium. CrossrefMedlineGoogle Scholar37. SMITHHOFMANN LA: Acquired hyperoxaluria, urolithiasis, and intestinal disease: a new digestive disorder? Gastroenterology 66:1257-1261, 1974 Increased intestinal absorption of oxalate is a primary factor causing calcium oxalate stones associated with intestinal fat malabsorption. Treatment includes low oxalate diet, cholestyramine, and, in some instances, oral calcium supplements to render oxalate nonabsorbable. CrossrefMedlineGoogle Scholar38. TOBIAN L: Hypertension and the kidney. Arch Intern Med 133:959-967, 1974 This review relates the extensive body of knowledge obtained from experimental models of hypertension to the various forms of hypertension in man. CrossrefMedlineGoogle Scholar39. KAPLAN N: The prognostic implications of plasma renin in essential hypertension. JAMA 231:167-170, 1975 A review of studies of possible correlation between plasma renin and vascular complications in essential hypertension. This analysis concludes that categorizing renin as a risk factor in the vascular complications of hypertension is not yet justified. CrossrefMedlineGoogle Scholar40. LARAGHSEALEYBUHLER JJF: The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. Am J Med 58:4-13, 1975 A current review is presented of this group's data and concepts of the relative roles of renin and extracellular fluid volume in the pathogenesis and therapeutic responses of various forms of renal hypertension. CrossrefMedlineGoogle Scholar41. BRAVOTARAZIDUSTAN ERH: Beta-adrenergic blockade in diuretic-treated patients with essential hypertension. N Engl J Med 292:66-70, 1975 In 20 carefully studied patients on long-term diuretic therapy, propranolol produced a significant decrease in blood pressure without necessarily lowering plasma renin. CrossrefMedlineGoogle Scholar42. FOSTERMAXWELLFRANKLIN JMS: Renovascular occlusive disease. Results of operative treatment. JAMA 231:1043-1048, 1975 Report of the Cooperative Study of Renovascular Hypertension in which 15 centers participated between the years 1961 and 1969. CrossrefMedlineGoogle Scholar43. HUNTSHIPSHARRISON JSE: Renal and renovascular hypertension. A reasoned approach to diagnosis and management. Arch Intern Med 133:988-999, 1974 A detailed analysis of the results of medical and surgical treatment of renal hypertension at the Mayo Clinic in a group of patients who entered the study between 1958 and 1965. CrossrefMedlineGoogle Scholar44. GIFFORDSTEWARTALFIDI RBR: Controlling atherosclerotic renovascular hypertension. Geriatrics 28:124-131, 1973 This is a brief review of the experience of the Cleveland Clinic group with renovascular hypertension due to arteriosclerotic disease of the renal arteries. MedlineGoogle Scholar45. LAZARUSHAMPERSMERRILL JCJ: Hypertension in chronic renal failure. Treatment with hemodialysis and nephrectomy. Arch Intern Med 133:1059-1066, 1974 The management of hypertension in chronic renal failure is summarized concisely. CrossrefMedlineGoogle Scholar46. MAMDANILIMMAHUKAR BVS: Recovery from prolonged renal failure in patients with accelerated hypertension. N Engl J Med 291:1343-1344, 1974 Five patients with accelerated hypertension and uremia underwent delayed recovery of renal function, so that hemodialysis could be discontinued 6 to 26 months after its initiation. CrossrefMedlineGoogle Scholar47. MCNEILADELSTEIN BS: Value of case finding in hypertensive renovascular disease. N Engl J Med 293:221, 1975 This paper and an accompanying one (293:216, 1975) attempt to determine the cost of finding and surgically treating renovascular hypertension as well as assessing the difference in outcomes of essential and renovascular hypertension treated by drug therapy. CrossrefMedlineGoogle Scholar48. MERRILL J: Glomerulonephritis. N Engl J Med 290:257-266; 313-319; 374-381, 1974 An excellent and up to date overview of various aspects of glomerulonephritis. CrossrefMedlineGoogle Scholar49. CAMERON J: Bright's disease today: the pathogenesis and treatment of glomerulonephritis. Br Med J 4:87-90; 160-163; 217-220, 1972 Excellent overviews of classification, clinical features, pathogenesis, pathology, and management of "glomerulonephritis." CrossrefMedlineGoogle Scholar50. WILSONDIXON CF: Immunopathology and glomerulonephritis. Ann Rev Med 25:83-98, 1974 A detailed review of the immunopathology of glomerulonephritis from a world-renowned laboratory. CrossrefMedlineGoogle Scholar51. BALDWINGLUCKSCHACHT DMR: The long term course of poststreptococcal glomerulonephritis. Ann Intern Med 8:342-358, 1974 A new look at a controversial subject. Poststreptococcal glomerulonephritis may be the starting point of the path leading to end-stage renal disease. LinkGoogle Scholar52. GUTMANSTRIKERGILLILAND RGB: The immune complex glomerulonephritis of bacterial endocarditis. Medicine (Baltimore) 51:1-25, 1972 A survey of the clinical features and pathogenetic mechanisms in the glomerulopathy associated with infective endocarditis. CrossrefMedlineGoogle Scholar53. WILSONDIXON CF: Antiglomerular basement membrane antibody induced glomerulonephritis. Kidney Int 3:74-89, 1973 The definitive description of clinical features associated with a true "auto-immune" glomerulonephritis—antiglomerular basement membrane antibody induced glomerulonephritis. CrossrefMedlineGoogle Scholar54. MCCOYABRAMOSKYTISHER RCC: IgA nephropathy. Am J Pathol 76:123-144, 1974 An excellent description of a newly described clinicopathologic entity, also known as Berger disease. MedlineGoogle Scholar55. LLACHARIEFFMASSRY FAS: Renal vein thrombosis and nephrotic syndrome: a prospective study of 36 adult patients. Ann Intern Med 83:8-14, 1975 Additional evidence that renal vein thrombosis is a complication and not a cause of nephrotic syndrome. The next question is what can be done to prevent its occurrence. LinkGoogle Scholar56. CAMERONTURNEROGG JDC: The nephrotic syndrome in adults with "minimal change" glomerular lesions. Q J Med 43:461-488, 1974 A comprehensive look at a renal lesion more frequent in children, but which remains as an important pathologic entity in adults with nephrotic syndrome. MedlineGoogle Scholar57. KASHGARIANHAYSLETTSIEGEL MJN: Lipoid nephrotis and focal sclerosis. Distinct entities or spectrum of disease (editorial). Nephron 13:105-108, 1974 This editorial, as well as a companion paper (Nephron 13:138-144, 1974), proposes that lipoid nephrosis and focal glomerular sclerosis are a part of a spectrum of the same disease. CrossrefMedlineGoogle Scholar58. ERWINDONADIOHOLLEY PJK: The clinical course of idiopathic membranous nephropathy. Mayo Clinic Proc 48:697-713, 1973 A thorough analysis of a well studied group of patients, demonstrating the lack of effects of steroid therapy on the natural history of the disease. MedlineGoogle Scholar59. ROWCAMERONTURNER PJD: Membranous nephropathy. Long term follow-up and association with neoplasia. Q J Med 44:207-239, 1975 Membranous nephropathy in an adult with nephrotic syndrome may be a clue to underlying malignant disease. MedlineGoogle Scholar60. GINZLERNICASTRICHEN EAC: Progression of mesangial and focal to diffuse lupus nephritis. N Engl J Med 291:693-696, 1974 This paper as well as a companion paper (Lab Invest 32:665-672, 1975) is concerned with observations seem to modify previous optimism regarding the prognostic role of renal biopsies in lupus nephritis. CrossrefMedlineGoogle Scholar61. WOLFFFANCIHORN SAR: Wegener's granulomatosis. Ann Intern Med 81:513-525, 1974 An excellent National Institutes of Health review of a relatively rare disease, but one of the very few that have yielded to immunosuppressive therapy. LinkGoogle Scholar62. KYLEBAYRD RE: Amyloidosis: review of 236 cases. Medicine (Baltimore) 54:271-300, 1975 A report of a large series of primary and secondary amyloidosis. Contains a good store of useful clinical information on diagnosis and prognosis. CrossrefMedlineGoogle Scholar63. MURRAYGOLDBERG TM: Chronic interstitial nephritis: etiologic factors. Ann Intern Med 82:453-459, 1975 A survey of a common form of renal disease; re-emphasizes the rarity of bacterial infection and the importance of analgesic abuse as etiologic factors. LinkGoogle Scholar64. LEHMANWILSONDIXON DCF: Extraglomerular immunoglobulin deposits in human nephritis. Am J Med 58:765-786, 1975 The techniques that have elucidated so much about glomerular disease are being applied to tubulointerstitial disease as exemplified by this survey of renal biopsy material. Immunologic factors appear to play a role in tubulointerstitial injury. CrossrefMedlineGoogle Scholar65. BRICKERKLAHR NS: Obstructive nephropathy, in Diseases of the Kidney, 2nd ed., edited by STRAUSS MB, WELT LG. Boston, Little, Brown and Co., 1971, pp. 997-1037. General review with a detailed analysis of the functional consequences of urinary tract obstruction. Google Scholar66. GILLENWATERWESTERVELTVAUGHAN JFE: Renal function after release of chronic unilateral hydronephrosis in man. Kidney Int 7:179-186, 1975 Recent and complete description of the functional abnormalities seen after correction of partial unilateral ureteral obstruction in 10 patients. CrossrefMedlineGoogle Scholar67. VAUGHANBUHLERLARAGH EFJ: Normal renin secretion in hypertensive patients with primarily unilateral chronic hydronephrosis. J Urol 112:153-156, 1974 In contrast to the conclusions reported in previous papers, the data in this report suggest that hypertension in chronic hydronephrosis in its established state may not be caused by increased renin secretion. CrossrefMedlineGoogle Scholar68. ELKINSGOLDMANMENG MSC: Ureteral obstruction in patients with uterine prolapse. Radiology 110:289-294, 1974 This report of 19 cases emphasizes for the first time in the American radiological literature the importance of uterine prolapse as a cause of obstructive nephropathy. CrossrefMedlineGoogle Scholar69. BEWICKCOLLINSSAXTON MRH: The surgery and problems of ureter in human renal transplantation. Br J Urol 46:493-510, 1974 As the number of renal transplants increases some of these cases will be seen by the internist. This is an excellent review of urological complications associated with 200 consecutive renal transplants. CrossrefMedlineGoogle Scholar70. HARRINGTONCOHEN JJ: Current concepts: acute oliguria. N Engl J Med 292:89-91, 1975 A concise review of acute oliguric states with emphasis on the diagnosis and management of acute tubular necrosis. CrossrefMedlineGoogle Scholar71. PHILLIPSEASTWOODCURTIS MJJ: Tetracycline poisoning in renal failure. Br Med J 2:149-151, 1974 Administration of tetracycline to patients with renal insufficiency has harmful antianabolic or catabolic effects, and may possibly result in deterioration of renal function. CrossrefMedlineGoogle Scholar72. DIAZ-BUXOWAGONERHATTERY JRR: Acute renal failure after excretory urography in diabetic patients. Ann Intern Med 83:155-158, 1975 There may be exceptional risk to excretory urography for patients with diabetic nephropathy, as well as those with multiple myeloma or hypersensitivity to radiographic contrast agents. LinkGoogle Scholar73. FINKELSTEINKASHGARIANHAYSLETT FMJ: Clinical spectrum of postpartum renal failure. Am J Med 57:649-654, 1974 This syndrome of microangiopathic hemolytic anemia and renal failure due to intravascular coagulation may not be invariably irreversible as previously reported. CrossrefMedlineGoogle Scholar74. GROSSMANHAMILTONMORSE RRB: Nontraumatic rhabdomylosis and acute renal failure. N Engl J Med 291:807-811, 1974 Myoglobinuric acute renal failure, well known with major traumatic injury, also occurs in patients with myopathy, convulsions, strenuous exercise, and viral illness. It may cause hypocalcemia and rebound hypercalcemia. CrossrefMedlineGoogle Scholar75. ABELBECKABBOTT RCW: Improved survival from acute renal failure after treatment with intravenous essential L-amino acids and glucose. N Engl J Med 288:695-699, 1973 Hyperalimentation appeared to hasten recovery from complicated oliguric acute renal failure and to improve survival. These controlled-study data require confirmation before widespread clinical use of hyperalimentation can be recommended for patients with acute renal failure. CrossrefMedlineGoogle Scholar76. SIEGLERBLOOMER RH: Acute renal failure with prolonged oliguria: an account of five cases. JAMA 225:133-136, 1973 Oliguria for 31 to 72 days yet sufficient recovery of renal function so that continued dialysis was unnecessary. Prolonged oliguria in acute tubular necrosis (and in lupus nephritis and malignant hypertension) does not preclude recovery; dialysis should not be discontinued prematurely. CrossrefMedlineGoogle Scholar77. DEFRONZOHUMPHREYWRIGHT RRJ: Acute renal failure in multiple myeloma. Medicine (Baltimore) 54:209-223, 1975 Acute renal failure in myeloma, although less common than slowly progressive chronic renal failure, is an important complication; in most patients it is theoretically preventable by treating hypercalcemia, volume depletion, or avoiding nephrotoxic antibiotics or pyelographic dye. CrossrefMedlineGoogle Scholar78. BRICKER N: Adaptations in chronic uremia: pathophysiologic "trade-offs." Hosp Prac 9:119-126, 1974 Expanding on the "intact nephron hypothesis" (homeostasis in renal failure is achieved by increasing function of remaining nephrons), Bricker formulates the "trade-off" hypothesis (uremia results from adaptations which sustain solute excretion). CrossrefGoogle Scholar79. BENNETTSINGERCOGGINS WIC: A guide to drug therapy in renal failure. JAMA 230:1544-1553, 1974 An extraordinarily useful set of tables listing recommended maintenance dose intervals for drugs, modification of dosage with dialysis, and toxic effects of the drugs in patients with renal insufficiency. CrossrefMedlineGoogle Scholar80. Anaemia in chronic renal failure (editorial). Lancet 1:959-960, 1975 A succinct summary of mechanisms and thus possible approaches to the therapy of the anemia of chronic renal failure. MedlineGoogle Scholar81. WALSER M: Treatment of renal failure with ketoacids. Hosp Prac 9:59-66, 1975 This paper summarizes in palatable form recent research of fundamental importance in the field of protein (nitrogen) metabolism. CrossrefGoogle Scholar82. BURTON B: Current concepts of nutrition and diet in diseases of the kidney. I. General principles of dietary management. II. Dietary regimen in specific kidney disorders. J Am Diet Assoc 65:623-633, 1974 A thorough review of diet in renal disease including the use of low-quantity, high-quality protein in the treatment of renal failure. CrossrefMedlineGoogle Scholar83. DEFRONZOANDRESEDGAR RRP: Carbohydrate metabolism in uremia: a review. Medicine (Baltimore) 52:469-481, 1973 Multiple abnormalities of carbohydrate metabolism are described in uremia including peripheral insulin antagonism, inhibition of insulin secretion, hypokalemic inhibition of insulin secretion, and diminished degradation of insulin. CrossrefMedlineGoogle Scholar84. KJELLSTRANDSHIDEMANSIMMONS CJR: Renal transplantation in insulin-dependent diabetic patients. Kidney Int 6:515-520, 1974 Deals with a form of renal disease that accounts for approximately one third of patients who would die of end-stage renal failure were it not for dialysis and transplantation, treatment that until recently has not generally been provided to diabetic patients. Google Scholar85. KNEPSHIELDSCHREINERLOWENTHAL JGD: Dialysis of poisons and drugs—annual review. Trans Am Soc Artif Intern Organs 19:590-633, 1973 The best reference when caring for a critically ill patient with an overdose of a known drug or ingestion of a known poison and when one wants to know whether dialysis might be helpful. CrossrefMedlineGoogle Scholar86. TENCKHOFF H: Peritoneal dialysis today: a new look. Nephron 12:420-436, 1974 This review indicates that recent advances make peritoneal dialysis a reasonable treatment for some patients with end-stage renal disease as well as for acute, self-limited problems. CrossrefMedlineGoogle Scholar87. CHANG T: Microencapsulated absorbent hemoperfusion for uremia, intoxication and hepatic failure. Kidney Int 7:387S-392S, 1975 Research through two decades with membrane-coated activated charcoal has reached the stage of clinical investigation in humans; one of the more promising technical innovations in dialysis. Google Scholar88. BAGDADE J: Atherosclerosis in patients undergoing maintenance hemodialysis. Kidney Int 7:370S-372S, 1975 Atherosclerosis accounts for the majority of deaths in chronic dialysis patients, especially after the first two years. A review of a number of factors and mechanisms that may be responsible for the accelerated atherosclerosis in these patients. Google Scholar89. GROSSKEANEMCDONALD JWA: Survival and rehabilitation of patients on home hemodialysis: five years' experience. Ann Intern Med 78:341-346, 1973 This paper summarizes the survival and rehabilitation of 628 patients dialyzed at home under the direction of 12 home-dialysis training centers. LinkGoogle Scholar90. SZMUNESSPRINCEGRADY WAG: Hepatitis B infection: a point-prevalence study in 15 U.S. hemodialysis centers. JAMA 227: 901-906, 1974 Hepatitis B infection is common not only in chronic hemodialysis patients (51%) and staff (34%) but also in household family contacts of infected patients (61%). A national trial of hepatitis B immune globulin is underway. CrossrefMedlineGoogle Scholar91. COMTYCOHENSHAPIRO CSF: Pericarditis in chronic uremia and its sequels. Ann Intern Med 75:173-183, 1971 Pericarditis occurred in 25 of 152 chronically dialyzed patients, three of whom died. In another series, 13 of 17 patients developed pericarditis within two months of starting dialysis: MARINI PV, HULL AR in Kidney Int 7 (suppl):163S-166S, 1975 LinkGoogle Scholar92. SCRIBNERBABB BA: Evidence for toxins of "middle" molecular weight. Kidney Int 7:349S-351S, 1975 Although the hypothesis that "middle" (molecular weight 500-5000) molecules are the toxins of uremia (specifically of uremic neuropathy) is unproved, it has stimulated interest, controversy, and research; this brief paper deserves reading. Google Scholar93. KERSHKRONFELDUNGER ESA: Autonomic insufficiency in uremia as a cause of hemodialysis-induced hypotension. N Engl J Med 290:650-653, 1974 Of eight patients with severe hypotension during hemodialysis, six were found to have autonomic dysfunction and peripheral neuropathy. Hypotension in these patients did not respond to volume expansion but did respond to norepinephrine. CrossrefMedlineGoogle Scholar94. : The 12th report of the human renal transplant registry. JAMA 233:787-796, 1975 A necessary reference for advising patients about transplantation; unfortunately, reliable comparable data on results of chronic dialysis are not available. Data include survivals of patients and grafts from sibling, parent, and cadaver donors. CrossrefMedlineGoogle Scholar95. : Renal transplantation in congenital and metabolic diseases. JAMA 232:148-153, 1975 Current data on results of transplantation in relatively common disorders (diabetes, lupus erythematosus), not common disorders (familial nephritis, Alport syndrome, medullary cystic disease, gout), and uncommon conditions (amyloidosis, cystinosis, Fabry disease, and oxalosis). CrossrefMedlineGoogle Scholar96. MANNICK J: Clinical kidney transplantation: areas of current interest. Postgrad Med 54:171-176, 1973 A lucid and concise exposition of the clinical immunology of renal transplantation. CrossrefMedlineGoogle Scholar97. OPELZTERASAKI GP: Tissue typing in renal transplantation. Contemp Surg 5:11-17, 1974 A straightforward description of HL-A (human leukocyte antigen), MLC (mixed leukocyte culture) and "crossmatch" (lymphocytotoxin) histocompatibility testing. Google Scholar98. MERRILL J: Present status of kidney transplantation. DM 1-30, November 1974 A comprehensive review of human renal transplantation. Google Scholar99. DAUSSETHORSBUSSON JJM: Serologically defined HL-A antigens and long term survival of cadaver kidney transplants: a joint analysis of 918 cases performed by France-Transplant and the London-Transplant Group. N Engl J Med 290:979-984, 1974 Data from France and England strongly supportive of the practice of HL-A matching for cadaveric renal transplantation. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: MEDICAL KNOWLEDGE SELF-ASSESSMENT PROGRAM IV AMERICAN COLLEGE OF PHYSICIANS Philadelphia, Pennsylvania*Robert W. Schrier, M.D., Chairman; Jack W. Coburn, M.D.; Jordan Cohen, M.D.; Richard J. Glassock, M.D.; Saulo Klahr, M.D.; Donna McCurdy, M.D.; Keith M. McDonald, M.D.; and Ronald B. Miller, M.D.Reprints are not available.†Computer literature-file of the National Library of Medicine, Bethesda, Maryland, consulted through the Regional Medical Library service Library of the College of Physicians of Philadelphia, with the technical assistance of Ruthanne Henner. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byReading in Internal MedicineRUSSELL M. WILDER, M.D., F.A.C.P. 1 January 1976Volume 84, Issue 1Page: 104-109KeywordsComputersLibrariesNephrology ePublished: 1 December 2008 Issue Published: 1 January 1976 PDF downloadLoading ...