Formation Of Renal Calculi Research Articles

THE EFFECT OF ORAL SODIUM PHOSPHATE ON THE FORMATION OF RENAL CALCULI AND ON IDIOPATHIC HYPERCALCURIA

THE EFFECT OF ORAL SODIUM PHOSPHATE ON THE FORMATION OF RENAL CALCULI AND ON IDIOPATHIC HYPERCALCURIA

Human renal calculus formation and magnesium.

Human Renal Calculus Formation and Magnesium Get access Nutrition Reviews, Volume 24, Issue 2, February 1966, Pages 43–46, https://doi.org/10.1111/j.1753-4887.1966.tb08352.x Published: 01 February 1966

The Composition and Mode of Formation of Renal Calculi

The Composition and Mode of Formation of Renal Calculi

Diagnostic considerations in hypercalcemia; with a discussion of the various means by which such a state may develop.

DESPITE knowledge that hypercalcemia, regardless of cause, is injurious and potentially lethal, there is wide variation in the diligence with which its presence or absence is determined in patients having suggestive manifestations of this disorder. A persistently high concentration of serum calcium is conducive to renal damage, calculus formation and vicarious calcification.1 , 2 In addition, anorexia, nausea and vomiting are exceedingly common complaints of patients with hypercalcemia, and physicians need be aware that such symptoms may herald the onset of a rapidly fatal course. Indeed, in those with markedly increased concentrations of serum calcium (usually in the range of 15 to . . .

Renal lymphatics. III. Clinical implications and experiments of nature.

Excerpt In previous publications1, 2the function of renal lymphatics in homeostasis of the kidney is discussed. We believe that the renal lymphatics act as a "safety valve" for the kidneys under co...

Urinary Excretion of Citrate in Humans Following Administration of Acetazolamide (Diamox)

Citrate is excreted in comparatively large amounts in human urine, and its excretion varies with age, diet, sex, and other factors from 100 to 1500 mg. per day. 1-4 It is lower in infants and children as compared with adults. 1-3,5-7 Citrate excretion is decreased by acidosis 7-12 (dietary, uremic, and diabetic) and by testosterone administration. 13 It is increased in alkalosis 7-12 and by the administration of estrogens, 14,15 parathyroid extract, 2,16,17 and vitamin D. 18-22 Previous experimental and clinical studies have suggested that urinary citrate aids in the chelation of calcium into a soluble complex. Low citrate levels in the presence of normal calcium-phosphorous ratios may play a role in the formation of renal calculi.2,23,24 In addition, citrate therapy has been reported to have induced an apparent improvement in a case of nephrocalcinosis. 25 In rats, acetazolamide administration has been observed to result in the deposition of calcium

Effect of acetazolamide on citrate excretion and formation of renal calculi.

ÖSTBERG,1 in 1931, suggested that the citric acid in urine functions to keep relatively insoluble calcium salts in solution. Since that time evidence has accumulated that in man the urinary citrate-calcium balance is an important mechanism for preventing the development of calcium calculi in the urinary tract.2 3 4 5 Additional evidence substantiating this concept has recently been provided by Harrison and Harrison.6 These investigators found that the urinary excretion of citrate was markedly reduced in rats that had been fed acetazolamide (Diamox). Furthermore, precipitation of calcium salts in the urinary tract of these animals was a striking finding.Recently, we have had . . .

Effect of corticoids on the resistance of the kidney to an excess of phosphates.

In unilaterally nephrectomized rats, the substitution of 1.2% NaH2PO4 for drinking water rapidly produced marked calcium deposition in the pars intermedia of the kidney. This effect of the phosphate solution is enhanced by concurrent treatment with desoxycorticosterone acetate (DCA) and inhibited by cortisol acetate (COLA). The possible rôle of corticoids in the production of clinical nephrocalcinosis and renal calculus formation is briefly discussed.

The Effect of Temperature, Humidity and Dehydration on the Formation of Renal Calculi

No AccessJournal of Urology1 Feb 1956The Effect of Temperature, Humidity and Dehydration on the Formation of Renal Calculi Charles L. Prince, Peter L. Scardino, and Casimir T. Wolan Charles L. PrinceCharles L. Prince More articles by this author , Peter L. ScardinoPeter L. Scardino More articles by this author , and Casimir T. WolanCasimir T. Wolan More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)66798-3AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1956 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited byEVANS K and COSTABILE R (2018) TIME TO DEVELOPMENT OF SYMPTOMATIC URINARY CALCULI IN A HIGH RISK ENVIRONMENTJournal of Urology, VOL. 173, NO. 3, (858-861), Online publication date: 1-Mar-2005.Sarmina I, Spirnak J and Resnick M (2018) Urinary Lithiasis in the Black Population: An Epidemiological Study and Review of the LiteratureJournal of Urology, VOL. 138, NO. 1, (14-17), Online publication date: 1-Jul-1987.Prince C and Scardino P (2018) A Statistical Analysis of Ureteral CalculiJournal of Urology, VOL. 83, NO. 5, (561-565), Online publication date: 1-May-1960.Flesch W (2018) Air Disimpaction of Ureteral CalculiJournal of Urology, VOL. 81, NO. 1, (96-96), Online publication date: 1-Jan-1959.Frank M, Vries A, Atsmon A, Lazebnik J and Kochwa S (2018) Epidemiological Investigation of Urolithiasis in IsraelJournal of Urology, VOL. 81, NO. 4, (497-505), Online publication date: 1-Apr-1959. Volume 75Issue 2February 1956Page: 209-215 Advertisement Copyright & Permissions© 1956 by The American Urological Association Education and Research, Inc.MetricsAuthor Information Charles L. Prince More articles by this author Peter L. Scardino More articles by this author Casimir T. Wolan More articles by this author Expand All Advertisement PDF downloadLoading ...

Disease of ureteral remnant following nephrectomy.

PATIENTS who have recurring urological symptoms following nephrectomy present a special problem to the practitioner. In many cases, nephrectomy has been done for pyohydronephrosis, calculus formation, or other obvious pathology, yet the symptoms for which the patient consulted his physician persist or sometimes recur many years after the operation. We would like to reemphasize the possibility of an abnormal or diseased remaining lower ureteral segment as a possible cause for the continued symptoms. In conditions such as papillary carcinoma of the renal pelvis and carcinoma of the ureter, removal of the entire ureter at the time of nephrectomy is universally considered the operation of choice. But in many cases, such as nephrectomy for renal tuberculosis, pyohydronephrosis, and renal calculus formation, the advisability of total nephroureterectomy is controversial. In the past few years, interest in the fate of the ureteral stump following nephrectomy has been kindled by experimental studies 1 and

A new theory on the formation of renal calculi.

SUMMARY 1. This paper presents a new theory on the formation and growth of urinary calculi based on the lymphatic drainage of the kidney which is described. 2. The material and methods which have been used in studying the formation of renal calculi have been described in detail. These include the technique of microradiography. 3. The current theories of stone formation from the smallest crystalline deposits are reviewed. 4. Observations have been made which are not explained by Randall's theory. 5. By the new theory all the observed facts, including the formation of Randall's plaques, can be explained. 6. Diffraction X-ray analysis has been used to support this new theory. 7. Facts of importance in partial nephrectomy in the treatment of renal lithiasis are emphasised and explained.

THE URINARY CITRATE EXCRETION IN PATIENTS WITH RENAL CALCULI

SummaryIt has been suggested that an important factor in the formation of renal calculi is a deficiency of citrate excretion by the kidney. This we have failed to confirm and consider rather that any gross diminution of urinary citrate is due simply to infection of the urinary tract. The proof of this is as follows:‐1. In seven patients with calculi and a sterile tract the average citrate content of the urine was comparable with that found in controls.2. Seven patients with calculi, associated with infection, were all found to have less citrate in their urine than normals.3. Experiments in vitro confirmed that in this latter group citrate was destroyed particularly by E. colz, although with Kosers medium this splitting action was not detectable.

THE RECOGNITION OF PRIMARY HYPERPARATHYROIDISM

The discovery that hyperparathyroidism is the cause of generalized osteitis fibrosa cystica has led to a widespread assumption that hyperparathyroidism manifests itself only as a disease of bone. 1 Because osteitis fibrosa cystica is a great rarity, it has been assumed that hyperparathyroidism is equally rare. Both of these assumptions have been proved to be false but they have nonetheless persisted. In 1934 Albright and his associates 2 at the Massachusetts General Hospital reported 17 proved cases of hyperparathyroidism, most of which they had observed during a period of two years. Analysis of these cases led them to conclude that (1) hyperparathyroidism can occur without evident disease of bone, (2) involvement of the urinary tract is a more common and more important manifestation of hyperparathyroidism than involvement of the skeleton, (3) hyperparathyroidism is relatively common and (4) it is the etiologic factor in the formation of renal calculi in an

THE FORMATION OF RENAL CALCULI IN BEDRIDDEN PATIENTS

My purpose in this paper is to call attention to, and illustrate by the report of cases, the effects of inadequate renal drainage and of phosphaturia in the formation of renal calculi in bedridden patients. In my experience it has been the phosphatic stones (calcium phosphate) which have produced the most serious results, because they can form rapidly and without symptoms, so that they may have already produced a serious condition when they are discovered. The fact that renal calculi are frequently formed in patients having paralyses which produce disturbances of urination, such for example as fractures of the spine and poliomyelitis, has been so generally recognized and so frequently reported that it is unnecessary to devote any space here to confirming it. The discussions concerning preventive treatment have emphasized the correction of metabolic disturbances, the relief of urinary obstruction, the removal of foci of infection, regulation of the diet

The Incidence of Urinary Tract Obstruction in Renal Calculus Formation

The Incidence of Urinary Tract Obstruction in Renal Calculus Formation

THE RELATION OF PROLONGED IMMOBILIZATION AND URINARY TRACT INFECTION TO RENAL CALCULUS FORMATION

Summary 1. The literature on the subject of prolonged immobilization in relation to renal calculus formation is reviewed and six illustrative cases are reported. 2. The mechanism of calculus formation and the influence exerted thereon by urinary tract infection and prolonged immobilization are considered. 3. Insoluble crystalloids which may appear as a urinary deposit are probably prevented from crystallizing out under normal conditions rather by the fact that in a clear urinethey have very little existence as such, due to the formation of soluble complex salts, than by the “protective action” of the urinary colloids. 4. The first stage in the formation of a calculus is the deposition of crystals within the urinary passages. 5. For a calculus to develop, mechanical conditions must be such that this deposit can be retained in the urinary tract for an adequate period. 6. Under normal conditions, such stasis may occur only in the lowest renal calyx, while if urinary obstruction exists it may occur anywhere in the urinary tract. 7. A urinary infection leads to accelerated growth of calculi, but cannot alone be responsible for their formation. 8. In the presence of stasis a urea-splitting infection may by the deposition of crystals initiate calculus formation, while a non-urea-splitting infection, by providing inflammatory products on which the primary deposition of crystals may occur, may, if the urine is already dangerously close to throwing down a deposit, thus indirectly initiate calculus formation. 9. Prolonged immobilization, by interfering with the drainage from the pelvis and calyces as a result of the position occupied by the kidneys, may provide sufficient time for the deposition of crystals which would otherwise not have been deposited till the urine had been voided, and cause these crystals to be retained, thus leading to calculus formation which would otherwise never have developed.

Rapid Formation of Renal Calculus

Rapid Formation of Renal Calculus