Metastatic bone tumors can lead to development of pathological fractures which may cause incessant pain. Hypercalcemia and hypercalciuria may develop secondary to skeletal metastasis and recumbency, leading to death from cardiac and renal sequeale. The proper surgical treatments of the metastatic bone tumor offer many advantages in relief of pain, simplifying nursing care, restoring resonable mobility and prevent complications. The authors reviewed 24 cases of metastatic bone tumors which received surgical treatment at Severance Hospital from January 1976 to March 1982. The results were obtained as follows: 1. Twenty four among three hundred patients with metastatic bone tumors were treated surgically. 2. There was no sexual preference and 66.7% were observed in the age of 51 to 70 group. 3. The most common site of operation was the femur. 4. The methods of operation were as follows: Resectionoflesion.....................5 Replacement with prosthesis..........3 Open reduction and internal..........10 Spinal fusion..........................2 Laminectomy............................4 5. All cases had received various types of ancillary treatment: radiation in 8 cases, 131I radioactive isotope in 1 case, chemotherapy in 2 cases, hormone therapy in 1 case, radiation and chemotherapy in 3 cases and conservative pain control in 9 cases. 6. Among the 15 followed cases, nine survived more than 6 months and 3 cases longer than 1 year after surgery. The pain was relieved markedly in twenty-three patients, and ambulated well with brace support.
Braces ; Drug Therapy ; Femur ; Fractures, Spontaneous ; Humans ; Hypercalcemia ; Hypercalciuria ; Neoplasm Metastasis ; Nursing Care

PURPOSE: The lithogenic risk factors were compared between the first time stone patients and recurrent stone patients according to age and gender. MATERIALS AND METHODS: We performed stone metabolic studies on first time stone formers (67 men and 42 women) and the recurrent stone formers (40 men and 20 women). We analyzed the groups' excretion differences for the lithogenic and inhibitory constituents such as calcium, uric acid, oxalate, sodium and citrate; we measured volume from the 24-hour urine samples and calcium, uric acid, sodium, potassium, chloride and phosphate from the serum samples. Hypercalciuria, hyperoxaluria, hypocitraturia and a low 24-hour urine volume (<1,500ml) were compared between the two groups according to age and gender. RESULTS: Hypocitraturia was the most common metabolic abnormality in all the groups. The incidence of hypocitraturia was higher in the recurrent stone formers (50.0%) than in the first time stone formers (48.6%), but this was not statistically significant. A low urine volume was shown to have more significant association (p<0.05) for recurrent stone formers (33.3%) compared to the first time stone formers (18.3%). CONCLUSIONS: Hypocitraturia was the most common lithogenic risk factor for stone patients. In the recurrent stone formers, a low urine volume is the risk factor that differentiates them from the first time stone formers.
Calcium ; Citric Acid ; Fluid Therapy ; Humans ; Hypercalciuria ; Hyperoxaluria ; Incidence ; Male ; Oxalic Acid ; Potassium ; Risk Factors* ; Sodium ; Uric Acid ; Urinary Calculi

We report three cases of cystinuria, presenting with urinary stones. A 2-year-old girl presented with urinary difficulty, hematuria, dysuria of sudden onset, and her 7-month-old younger brother also was presented with urinary difficulty, irritability on urination & stone passage. Other 6-month-old boy was admitted due to sudden onset anuria. They had radioopague renal & ureter stones and stone analysis revealed mixed cystine stones. The diagnosis of cystinuria was confirmed metabolic studies and stone analysis. Lrinary amino acid analysis showed excessive excretion of dibasic amino acids(cystine, ornithine, lysine, arginine). And they all had hypercalciuria and hyperuricosuria. They were treated with combination of percutaneous lithotripsy for large obstructing senes a nd an oral drug therapy with sodium bicarbonate for rendering the urine more alkaline, and alpha-mercaptopropionylglycine(ThiolaR). This form of treatment was sucessful in our three cases with elimination of recurrent nephrolithiasis, but in one patient, nephrotic syndrome possibly caused by ThiolaR was developed. The nephrotic syndrome was recovered spontaneously after cessation of Thiola. A review of literatures was also attempted briefly.
Anuria ; Child, Preschool ; Cystine ; Cystinuria* ; Diagnosis ; Drug Therapy ; Dysuria ; Female ; Hematuria ; Humans ; Hypercalciuria ; Infant ; Lithotripsy ; Lysine ; Male ; Nephrolithiasis ; Nephrotic Syndrome ; Ornithine ; Siblings ; Sodium Bicarbonate ; Tiopronin ; Ureter ; Urinary Calculi ; Urination

Animals ; Child ; Child, Preschool ; Chloride Channels ; genetics ; Dent Disease ; complications ; diagnosis ; genetics ; therapy ; Diuretics ; therapeutic use ; Humans ; Hydrochlorothiazide ; therapeutic use ; Hypercalciuria ; diagnosis ; genetics ; Mutation ; genetics ; Phosphoric Monoester Hydrolases ; genetics ; Proteinuria ; diagnosis ; etiology ; genetics

TRPV5 is believed to play an important role in the regulation of urinary calcium excretion. We assessed the effects of hydrochlorothiazide (HCTZ) on the expression of TRPV5, calbindin-D28K, and several sodium transporters in hypercalciuric rats. Sprague- Dawley rats were divided into 4 groups; control, HCTZ, high salt, and high salt with HCTZ group in experiment 1; control, HCTZ, high calcium (Ca), and high Ca with HCTZ group in experiment 2. To quantitate the expression of TRPV5, calbindin- D28K, and sodium transporters, western blotting was performed. In both experiments, HCTZ significantly decreased urinary calcium excretion. TRPV5 protein abundance decreased in all hypercalciuric rats, and restored by HCTZ in both high salt with HCTZ and high Ca with HCTZ group. Calbindin-D28K protein abundance increased in the high salt and high salt with HCTZ groups, but did not differ among groups in experiment 2. Protein abundance of NHE3 and NKCC2 decreased in all hypercalciuric rats, and were restored by HCTZ in only high Ca-induced hypercalciuric rats. In summary, protein abundance of TRPV5, NHE3, and NKCC2 decreased in all hypercalciuric rats. The hypocalciuric effect of HCTZ is associated with increased protein abundance of TRPV5 in high salt or calcium diet-induced hypercalciuric rats.
Animals ; Biological Transport ; Calcium/urine ; Calcium Channels/chemistry ; Calcium-Binding Protein, Vitamin D-Dependent/*biosynthesis ; Hydrochlorothiazide/pharmacology ; Hypercalciuria/*therapy ; Male ; Models, Biological ; Rats ; Rats, Sprague-Dawley ; Sodium/*metabolism ; Sodium-Hydrogen Antiporter/chemistry ; Sodium-Potassium-Chloride Symporters/metabolism ; TRPV Cation Channels/*biosynthesis/chemistry ; Thiazides/*pharmacology

Thiazide is known to decrease urinary calcium excretion. We hypothesized that thiazide shows different hypocalciuric effects depending on the stimuli causing hypercalciuria. The hypocalciuric effect of hydrochlorothiazide (HCTZ) and the expression of transient receptor potential vanilloid 5 (TRPV5), calbindin-D(28K), and several sodium transporters were assessed in hypercalciuric rats induced by high calcium diet and vitamin D3. Urine calcium excretion and the expression of transporters were measured from 4 groups of Sprague-Dawley rats; control, HCTZ, high calcium-vitamin D, and high calcium-vitamin D with HCTZ groups. HCTZ decreased urinary calcium excretion by 51.4% in the HCTZ group and only 15% in the high calcium-vitamin D with HCTZ group. TRPV5 protein abundance was not changed by HCTZ in the high calcium-vitamin D with HCTZ group compared to the high calcium-vitamin D group. Protein abundance of NHE3, SGLT1, and NKCC2 decreased in the hypercalciuric rats, and only SGLT1 protein abundance was increased by HCTZ in the hypercalciuric rats. The hypocalciuric effect of HCTZ is attenuated in high calcium and vitamin D-induced hypercalciuric rats. This attenuation seems to have resulted from the lack of HCTZ's effect on protein abundance of TRPV5 in severe hypercalciuric condition induced by high calcium and vitamin D.
Animals ; Calcium/therapeutic use/urine ; Calcium Channels/genetics/metabolism ; Cholecalciferol/*toxicity ; Hydrochlorothiazide/*therapeutic use ; Hypercalciuria/chemically induced/*drug therapy ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride Symporter Inhibitors/*therapeutic use ; Sodium-Glucose Transporter 1/genetics/metabolism ; Sodium-Hydrogen Antiporter/genetics/metabolism ; Sodium-Potassium-Chloride Symporters/genetics/metabolism ; TRPV Cation Channels/genetics/metabolism