Effects of Orthosiphon grandiflorus, Hibiscus sabdariffa and Phyllanthus amarus extracts on risk factors for urinary calcium oxalate stones in rats.

PURPOSE: We evaluated the antilithic effect of Orthosiphon grandiflorus, Hibiscus sabdariffa and Phyllanthus amarus extracts on known risk factors for calcium oxalate stones in rats. MATERIALS AND METHODS: We divided 30 male Wistar rats into 5 equal groups. Controls were fed a standard diet and the remaining groups received a 3% glycolate diet for 4 weeks to induce hyperoxaluria. One glycolate fed group served as the untreated group and the others were given oral extracts of Orthosiphon grandiflorus, Hibiscus sabdariffa or Phyllanthus amarus at a dose of 3.5 mg daily. We collected 24-hour urine and blood samples. Kidneys were harvested for histological examination. We measured the renal tissue content of calcium and oxalate. RESULTS: The Hibiscus sabdariffa group showed significantly decreased serum oxalate and glycolate, and higher oxalate urinary excretion. The Phyllanthus amarus group showed significantly increased urinary citrate vs the untreated group. Histological examination revealed less CaOx crystal deposition in the kidneys of Hibiscus sabdariffa and Phyllanthus amarus treated rats than in untreated rats. Those rats also had significantly lower renal tissue calcium content than untreated rats. All parameters in the Orthosiphon grandiflorus treated group were comparable to those in the untreated group. CONCLUSIONS: Hibiscus sabdariffa and Phyllanthus amarus decreased calcium crystal deposition in the kidneys. The antilithic effect of Hibiscus sabdariffa may be related to decreased oxalate retention in the kidney and more excretion into urine while that of Phyllanthus amarus may depend on increased urinary citrate. In contrast, administering Orthosiphon grandiflorus had no antilithic effect.

Effect of potassium depletion on urinary stone risk factors in Wistar rats.

Various studies have suggested that potassium depletion leads to acidosis and hypocitraturia. In Northeastern Thailand, for example, mild hypokalemia and mild hyperoxaluria are observed in most stone formers. However, there are limited reports about the direct link between potassium depletion and the formation of urinary stones, most of which are calcium oxalate stones. Therefore, we studied the direct effect of potassium depletion on the risk factors for calcium oxalate stone formation. Seventy-two rats were fed a control diet or a potassium-deficient diet for 1, 2, or 3 weeks (n = 12 per group). Twenty-four-hour urine collection was done for the measurement of potassium, calcium, oxalate, glycolate, citrate, phosphorus, and magnesium. Lactate dehydrogenase activity was also measured in order to assess renal tubular damage, and kidneys were harvested for histological examination. Furthermore, urinary supersaturation of calcium oxalate was calculated. With potassium depletion, the urinary concentrations of potassium, citrate, magnesium, and phosphorus decreased rapidly. There was no detectable renal damage, renal calcium deposition, and no significant increase of urinary oxalate or calcium. However, the urinary supersaturation index of calcium oxalate increased significantly in rats with potassium depletion. These findings indicate that potassium deficiency may increase the risk of stone formation through enhanced supersaturation.

Migration of a metal clip into the urinary bladder.

Migration of metal clips into the urinary tract is rare. We present a case in which migration of a metal clip into the urinary bladder occurred after retropubic radical prostatectomy. A 75-year-old man, who had undergone retropubic radical prostatectomy three years before, presented with painful micturition and gross hematuria. Radiography and cystoscopy showed two vesical stones. As treatment for these stones, transurethral holmium laser lithotripsy was performed. One of the stones had formed around a metal clip that had presumably migrated into the urinary bladder. After removal of both stones, the patient was able to void freely. In conclusion, it is important to remember that metal clips may migrate postoperatively and cause secondary complications. Therefore, metal clips should be applied sparingly at the vesicourethral anastomosis during retropubic radical prostatectomy.

Endogenous oxalogenesis after acute intravenous loading with ethylene glycol or glycine in rats receiving standard and vitamin B6-deficient diets.

OBJECTIVES: The effect on endogenous oxalate synthesis of acute intravenous loading with ethylene glycol or glycine was investigated in rats on a standard or a vitamin B6-deficient diet. METHODS: Twenty-four male Wistar rats weighing approximately 180 g were randomly divided into ethylene glycol and glycine groups of 12 animals each. These groups were further divided into two subgroups of six animals each that were fed either a standard or a vitamin B6-deficient diet for 3 weeks. Animals of these two subgroups received an intravenous infusion of 20 mg (322.22 micromol) of ethylene glycol or 100 mg (1332.09 micromol) of glycine, respectively. Urine samples were collected just before intravenous infusion of each substance and at hourly intervals until 5 h after receiving the infusion. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. RESULTS: Urinary oxalate and glycolate excretion was significantly increased after ethylene glycol administration. Significant differences between the control and vitamin B6-deficient groups were found. In contrast, there were only small changes of oxalate and glycolate excretion after glycine administration. Recovery of the given dose of ethylene glycol as oxalate in 5-h urine was 0.31% and 7.15% in the control and vitamin B6-deficient groups, respectively, whereas recovery of glycolate was 0.68% and 7.22%, respectively. CONCLUSIONS: Ethylene glycol loading has a significant effect on urinary oxalate excretion in both normal and vitamin B6-deficient rats, whereas glycine loading only has a small effect. Oxalate and glycolate excretion after ethylene glycol loading were respectively 23-fold and 11-fold higher in vitamin B6-deficient rats than in controls.

Oxalate synthesis from hydroxypyruvate in vitamin-B6-deficient rats.

We studied the effects of an intravenous hydroxypyruvate load on endogenous oxalogenesis in rats receiving a standard diet or a vitamin-B6-deficient diet. Twelve male Wistar rats were randomized to two groups and were fed either a standard diet or a vitamin-B6-deficient diet for 3 weeks. Then the animals received an intravenous infusion of 100 mg/ml (960.6 micromol/ml) of hydroxypyruvate slowly over 10 min. Urine samples were collected just before hydroxypyruvate infusion and at hourly intervals until 5 h afterward. Urinary oxalate, glycolate, and citrate levels were measured by capillary electrophoresis. Hourly urinary oxalate excretion peaked within 2 h, while urinary glycolate excretion peaked at 1 h, after the hydroxypyruvate load in both control and vitamin-B6-deficient rats. Both urinary oxalate and glycolate excretion were higher in vitamin-B6-deficient rats than in control rats. Infusion of hydroxypyruvate increased the 5-h urinary oxalate and glycolate excretion to 0.68% (6.56 micromol) and 0.53% (5.10 micromol) of the administered dose (mol/mol), respectively, in the control rats, while oxalate and glycolate excretion, respectively, increased to 2.43% (23.36 micromol) and 0.79% (7.59 micromol) of the dose in the vitamin-B6-deficient rats. Urinary citrate excretion was significantly lower at baseline and all other times in the vitamin-B6-deficient rats than in the control rats. In conclusion, a hydroxypyruvate load increased endogenous oxalate synthesis in control rats, and its synthesis was even greater in vitamin-B6-deficient rats. Vitamin B6 deficiency also resulted in significant hypocitraturia.

Gastrointestinal oxalic acid absorption in calcium-treated rats.

We studied whether urinary oxalate excretion after an acute oral load of oxalic acid is influenced by concomitant administration of calcium in rats. Male Wistar rats weighing approximately 180 g were divided into six groups of five animals each. After inducing anesthesia, the animals were orally (via a gastrostomy) given 110 micromol of oxalic acid along with 0, 27.5, 55, 110, or 220 micromol of calcium (0, 27.5, 55, 110, or 220 micromol Ca group, respectively). Saline was given to the control group instead of oxalic acid. Urine specimens were collected before administration and then at hourly intervals up to 5 h afterward. Urinary oxalate and citrate levels were measured by capillary electrophoresis, while urinary calcium, magnesium, and phosphorus levels were measured by ICP spectrophotometry. Urinary oxalate excretion peaked at 1 h after administration and was higher in the 0, 27.5, and 55 micromol Ca groups than in the control group. The urinary recovery of oxalate in these groups was 10-15%, while the recovery rate was less than 3% in other groups. Urinary Ca excretion showed no significant changes, either over time or between groups. Free oxalic acid is absorbed more readily from the gastrointestinal tract than calcium oxalate, while simultaneous administration of calcium appears to block intestinal oxalic acid absorption in a dose-dependent manner.

Urinary response to an oxalic acid load is influenced by the timing of calcium loading in rats.

PURPOSE: Dietary intake of calcium or dairy products has been shown to decrease urinary oxalate excretion by limiting its intestinal absorption. However, not enough attention has been given to whether there is any benefit from altering the schedule of ingesting calcium and oxalate. Therefore, we investigated the effects of changes in the timing of calcium and oxalate loading on urinary oxalate excretion. MATERIALS AND METHODS: Male Wistar rats weighing 180 to 200 gm were fasted and randomized into several groups. They were then administered normal saline or oxalic acid with or without calcium or milk. Calcium or milk was given immediately, or 5, 10, 15 or 30 minutes before or after the oxalate load. All treatments were given via gastrostomy. Urine samples were collected by bladder puncture just before administration and at hourly intervals up to 5 hours afterward. Urinary oxalate was measured by capillary electrophoresis. RESULTS: Urinary oxalate increased after the administration of oxalate alone, while it decreased when oxalate was combined with calcium or milk. Urinary oxalate showed a smaller increment when calcium or milk was given before than after oxalate loading, and it was much smaller when calcium or milk was given immediately before oxalate. CONCLUSIONS: Prior calcium loading appears to have a positive influence on decreasing oxalic acid absorption from the intestinal tract. Therefore, calcium or dairy products should always be ingested before a meal rich in oxalate to prevent oxalate absorption and decrease urinary oxalate excretion.

Urolithiasis in Okinawa, Japan: a relatively high prevalence of uric acid stones.

AIM: The aim of the present study was to investigate the composition of urinary tract stones in patients from Okinawa, the most southern island group of Japan. METHODS: The study was conducted by 12 hospitals in Okinawa. A total of 1816 urinary tract calculi were obtained from 1816 patients (1323 males; 493 females). The patients had a mean age of 53 +/- 15.3 years (mean +/- SD). The calculi were examined to determine their chemical composition. Stone samples were analyzed by computed infrared spectrophotometer. RESULTS: Pure stones comprised 58.4% of the total, with calcium oxalate stones accounting for 40% (21% monohydrate [whewellite]; 6.6% dihydrate [weddellite]; and 12.4% combined monohydrate and dihydrate stones), uric acid/urate stones for 9.6%, calcium phosphate stones for 5.1%, and struvite stones for 3.7%. The other 41.6% of the stones consisted of calcium oxalate mixed with other components. The male-to-female ratio was 2.7:1. CONCLUSION: In our series, calcium oxalate stones accounted for 81.6% of the urinary tract calculi, while uric acid/urate stones accounted for 15.8%. Uric acid stones, predominantly the anhydrous and/or dihydrate forms, showed a relatively high prevalence. Calcium oxalate stones, predominantly in the form of whewellite, showed a high prevalence among pure calculi; while the predominant combinations among mixed calculi were weddellite + calcium phosphate and whewellite + uric acid/urate.

Milk and calcium prevent gastrointestinal absorption and urinary excretion of oxalate in rats.

Dietary oxalate plays a very important role in the formation of calcium oxalate stones, and dietary intake of calcium may decrease oxalate absorption and its subsequent urinary excretion. The purpose of the present study was to determine the effect on urinary oxalate excretion of an acute oral calcium load, standard milk, or high-calcium low-fat milk followed by a dose of oxalic acid. Male Wistar rats weighing 180-200 g were divided into 7 groups of 6 rats each. All animals were fasted for about 24 hours, anesthetized, and hydrated with normal saline at 3-4 mL/hour. Then the animals were given 1 mL of normal saline [Control], 10 mg (111.1 micromol) of oxalic acid [Ox alone], 2 mL of standard milk (calcium: 1.16 mg or 29 micromol/mL) [NCa milk], 2 mL of high-calcium low-fat milk (calcium: 2.05 mg or 51.3 micromol/mL) [HCa milk], equimolar calcium (4.44 mg or 111 micromol) followed by 10 mg of oxalic acid [Ca + Ox], 2 mL of high-calcium low-fat milk followed by 10 mg of oxalic acid [HCa milk + Ox], or 2 mL of standard milk followed by 10 mg of oxalic acid [NCa milk + Ox]. All treatments were administered via a gastrostomy. Urine samples were collected by bladder puncture just before administration and at hourly intervals up to 5 hours afterwards. Urinary oxalate was measured by capillary electrophoresis, while urinary calcium, magnesium and phosphorus were measured by inductively coupled plasma spectrometry. Urinary oxalate excretion peaked at 1 hour in the Ox alone group, while it peaked at 2 or 3 hours in the Ca + Ox, HCa milk + Ox, and NCa milk + Ox groups. Urinary oxalate excretion decreased significantly when 10 mg of oxalate was administered immediately after the administration of equimolar calcium, high-calcium low-fat milk, or standard milk. The cumulative urinary oxalate excretion over 5 hours was approximately 13.6%, 3.5%, 1.6%, and 2.4% in the Ox alone, Ca + Ox, HCa milk + Ox, and NCa milk + Ox groups, respectively. In conclusions, this study demonstrated that calcium salt, or dairy products containing calcium (especially high-calcium low-fat milk) could decrease the gastrointestinal absorption and subsequent urinary excretion of oxalate.

Urinary oxalic acid excretion differs after oral loading of rats with various oxalate salts.

BACKGROUND: To compare urinary oxalate excretion after the oral administration of oxalic acid, disodium oxalate, or calcium oxalate in rats. METHODS: Male Wistar rats were divided into four groups of six rats each and were intravenously hydrated with normal saline, and then were administered normal saline (control group), 10 mg of oxalic acid, equimolar disodium oxalate, or equimolar calcium oxalate via a gastrostomy. Urine specimens were collected just before administration and at hourly intervals up to 5 h afterwards. The urinary oxalate, calcium, magnesium and phosphorus levels were measured. RESULTS: Urinary oxalate excretion peaked at 1-2 h after administration of oxalic acid or equimolar disodium oxalate, while administration of calcium oxalate only caused a small increase of urinary oxalate excretion. Cumulative urinary oxalate excretion during 5 h was 1.69 +/- 0.10 mg (mean +/- SD; 17%), 1.43 +/- 0.13 mg (13%), and 0.22 +/- 0.03 mg (2%) after the administration of oxalic acid, disodium oxalate, and calcium oxalate, respectively. Urinary calcium excretion showed a decrease in the oxalic acid and disodium oxalate groups, while urinary magnesium or phosphorus excretion did not change significantly. CONCLUSION: The upper gastrointestinal tract seems to be the major site of oxalic acid absorption and only free oxalate is absorbed irrespective of whether it is the sodium salt or not. After binding to calcium in the gut, oxalic acid absorption seems to be inhibited in the presence of calcium and this means that calcium oxalate is poorly absorbed (at least in the upper gastrointestinal tract).