No abstract available.
Carcinoma, Renal Cell* ; Nephrons*

No abstract available.
Animals ; Nephrons* ; Population Characteristics* ; Rats*

Renal hypoplasia is defined as a subnormal growth of the kidney with a distinct cortex and medulla and is recognizable as a kidney. It is known that renal hypoplasia can induce hypertension by reduction of functioning nephron. Patients with reduced functioning renal mass by surgical or medical causes have a risk to develop hypertension. Patients with congenital reduction of functioning nephron have more frequently showed renal insufficiency. But renal hypoplasia induced hypertension is very rare and reported rarely in international literature. We report two cases of hypertension associated with congenital renal hypoplasia.
Humans ; Hypertension* ; Kidney ; Nephrons ; Renal Insufficiency

No abstract available.
Animals ; Nephrons* ; Population Characteristics* ; Rats* ; Renin*

Effects of cadmium exposure on renal Na+ and K+ transports were studied in rats. During the course of cadmium treatment (2 mg Cd/kg/day, s.c. injections for 3 weeks) renal tubular transports of Na+ and K+ were evaluated by lithium clearance technique. During the early phase (first week) of cadmium treatment, urinary Na+ excretion decreased drastically and this was due to an increased Na+ reabsorption both in the proximal and distal nephrons. During the late phase (third week) of cadmium treatment, filtered Na+ load was decreased by reduction in GFR, but the renal Na+ excretion returned to the control level due to impaired Na+ transport in the proximal tubule. Urinary excretion of K+ did not change during the early phase, but it rose markedly during the late phase of cadmium treatment. These results indicate that a light cadmium intoxication induces a Na+ retention, and a heavy intoxication results in a K+ loss. Possible mechanisms for these changes are discussed.
Animals ; Cadmium* ; Lithium ; Nephrons ; Potassium* ; Rats* ; Sodium*

The maintenance of potassium balance depends primarily on excretion by the kidney. The regulated secretion of potassium normally accounts for most of urinary potassium excretion. Potassium transport along the nephron has two main features:the ubiquitous Na,K-ATPase defines basolateral membranes, whereas site-specific potassium transporters are responsible for the apical transport. Two different cell types mediate secretion and reabsorption of potassium. Principal cells secrete potassium, whereas intercalated cells, especially those belonging to the subfamily of beta-intercalated cells, reabsorb potassium. The factors that stimulate potassium secretion by the principal cells include (1) increased extracellular fluid potassium concentration (2) increased aldosterone and (3) increased tubular flow rate. One factor that decreases potassium secretion is increased hydrogen concentration (acidosis). In situations associated with severe potassium depletion, there is a cessation of potassium secretion and net reabsorption of potassium. It is believed that H,K-ATPase transport mechanism located in the luminal membrane of the cortical and outer medullary collecting duct cells reabsorb potassium in exchange for hydrogen secreted into the tubular lumen.
Acidosis ; Aldosterone ; Extracellular Fluid ; Hydrogen ; Kidney* ; Membranes ; Nephrons ; Phenobarbital ; Potassium*

The mesoblastic nephroma is a rare benign renal tumor that frequently appears as a neonatal abdominal mass. This benign tumor is composed primarily of connective tissue that growth between intact nephrons and often replaces most of the renal parenchyme. Contrast media within the calyceal systems are seen within the tumor representing function by nephrons trapped within the mass. Prognosis after complete excision is excellent.
Connective Tissue ; Contrast Media ; Nephroma, Mesoblastic* ; Nephrons ; Prognosis

Renal tubule and vasa recta are arranged in complex but specific anatomic relationships and the production of a concentrated urine is achieved by countercurrent multiplication mechanism in the renal medulla. This model requires that the ascending thin limb is highly permeable to NaCl but impermeable to water, while the descending thin limb is impermeable to NaCl but highly permeable to water. The single effect in the outer medulla is active NaCl reabsorption by the thick ascending limb of Henle, which is the primary energy source of urine concentration. On the other hand, the single effect for inner medullary concentration is the passive efflux of NaCl from the thin ascending limb, which requires a high concentration of interstitial urea that is reabsorbed from the terminal inner medullary collecting duct. The hypothesis has been supported by micorpuncture studies or isolated perfused tubule studies until early 1990s. In recent 10 years, many transport proteins involved in the urine concentrating mechanism have been cloned, which enabled us to understand how a concentrated urine is produced, how this process is regulated and the specific transport process that are involved, proving the countercurrent multiplication hypothesis. In this review, the transport properties of outer and inner medullary nephron segments and the transport proteins involved in the transport of NaCl, water(aquaporins), and urea(urea transporters) will be reviewed.
Carrier Proteins* ; Clone Cells ; Extremities ; Hand ; Nephrons ; Urea ; Water

The present experiment was designed to investigate renal function in conscious rabbits. Pentobarbital caused some reduction of urinary volume and hemohynamics, but the changes were not significant. UnaV, UkV, UclV were not changed by pentobarbital in dose of 3.0~9.0mg/kg i.v.. Urinary flow snd UclV were not changed by pentothal sodium, 5.0mg/kg i.v., but the UnaV and UclV increased from 30.61 to 66.19 uEq/min, from 28.29 to 62.91 uEq/min respectively, after pentothal sodium. There was no change in urinary potassium secretion after pentothal sodium. Left renal arterial infusion of pentothal sodium caused small changes in GFR, and clear increments of UnaV and UclV localized in that kidney in the urethane anesthetized rabbit. Natriuretic and chloruretic effect of pentothal sodium were not seen in mannitol diuresis. These data suggest that 1) the effects of pentobarbital and pentothal may not be the sam in conscious rabbit renal function, 2) natriuretic and chloruetic effect by pentothal may be caused by direct inhibition of sodium reabsorption in the distal nephron in the rabbit.
Diuresis ; Kidney ; Mannitol ; Nephrons ; Pentobarbital ; Potassium ; Rabbits* ; Sodium ; Thiopental ; Urethane

In an attempt to obtain evidence in the mechanism of stone formation, the effectiveness of Amiloride. a K-sparing diuretic known to act on the distal nephron. on the kidney with oxamide-induced urolithiasis was investigated. Futhermore. the influence of stone formation on the distribution of intrarenal blood flow and the effect of Amiloride on them were also studied. Most prominent derangements of renal function observed during stone formation were decreases of both C(PAH) and C(cr) indicating the curtailment in renal hemodynamics. The oxamide-treated kidney also responded to Amiloride with typical natriuresis and antikaluresis. in the same fashion with normal kidneys. The experiments in which the intrarenal blood flow distribution was measured by PAH-extraction technique raveled that mainly the cortical blood flow was curtailed, whereas non-cortical blood flow (medullary flow) did not change during oxamide-stone formation. Amiloride did not influence the intrarenal b100d flow distribution both in normal and oxamide kidneys. These observations suggest that oxamide-stone formation was initiated not by tubular necrosis produced by the toxic action of oxalate on the tubules, but rather by mechanical obstruction of the tubules.
Amiloride* ; Hemodynamics ; Kidney* ; Natriuresis ; Necrosis ; Nephrons ; Renal Circulation ; Urolithiasis