Summary of Renal Lymphatic Studies

Keyl, M. J.; Bell, Richard D.; Parry, William L.

doi:10.1016/s0022-5347(17)60418-x

Cited by 12 publications

(5 citation statements)

References 6 publications

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“…In contrast to these findings, Cuttino et al (1985) reported a medullary lymphatic system in pigs, Cockett (1977) in dogs and Ruszniják et al (1960) in rabbits. Animal studies examining content of renal lymph have shown that medullary interstitial fluid must contribute to hilar lymph ( Keyl et al, 1972 ), suggesting the presence of medullary lymphatics. However, fluid movement within the medullary interstitium to juxtamedullary lymphatics (in the cortex) can also cause this result ( Albertine and O’Morchoe, 1980 ; O’Morchoe and O’Morchoe, 1988 ).…”

Section: Anatomy Of Renal Lymphaticsmentioning

confidence: 99%

“…IRVP and interstitial fluid volume are the main drivers of renal lymph formation ( Bell et al, 1972 , 1974 ; Keyl et al, 1972 ). Clamping the renal artery causes decreased capsular lymph pressure that reflects decreased IRVP and tissue pressure ( Figure 5 ) ( Bell et al, 1972 ).…”

Section: Renal Lymphatic Physiology In Pathological Conditionsmentioning

confidence: 99%

“…Therefore, the increase in lymphatic pressure and flow seen in increased pelvic pressure is probably actually due to intra-renal venous obstruction secondary to the increased pelvic pressure. Increased pelvic pressure has been observed to obstruct venous outflow from the kidney due to the intimate intra-renal anatomical relationship between renal veins and pelvis ( Keyl et al, 1972 ; Holmes et al, 1977b ). In dogs, ureteric obstruction causes a diversion of hilar lymph to capsular lymph within 3 days due to compression of hilar lymphatics in the renal sinus by the distended renal pelvis ( Holmes et al, 1977b ).…”

Section: Renal Lymphatic Physiology In Pathological Conditionsmentioning

confidence: 99%

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Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

et al. 2019

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Renal lymphatics are abundant in the cortex of the normal kidney but have been largely neglected in discussions around renal diseases. They originate in the substance of the renal lobule as blind-ended initial capillaries, and can either follow the main arteries and veins toward the hilum, or penetrate the capsule to join capsular lymphatics. There are no valves present in interlobular lymphatics, which allows lymph formed in the cortex to exit the kidney in either direction. There are very few lymphatics present in the medulla. Lymph is formed from interstitial fluid in the cortex, and is largely composed of capillary filtrate, but also contains fluid reabsorbed from the tubules. The two main factors that contribute to renal lymph formation are interstitial fluid volume and intra-renal venous pressure. Renal lymphatic dysfunction, defined as a failure of renal lymphatics to adequately drain interstitial fluid, can occur by several mechanisms. Renal lymphatic inflow may be overwhelmed in the setting of raised venous pressure (e.g., cardiac failure) or increased capillary permeability (e.g., systemic inflammatory response syndrome). Similarly, renal lymphatic outflow, at the level of the terminal thoracic duct, may be impaired by raised central venous pressures. Renal lymphatic dysfunction, from any cause, results in renal interstitial edema. Beyond a certain point of edema, intra-renal collecting lymphatics may collapse, further impairing lymphatic drainage. Additionally, in an edematous, tense kidney, lymphatic vessels exiting the kidney via the capsule may become blocked at the exit point. The reciprocal negative influences between renal lymphatic dysfunction and renal interstitial edema are expected to decrease renal function due to pressure changes within the encapsulated kidney, and this mechanism may be important in several common renal conditions.

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Section: Anatomy Of Renal Lymphaticsmentioning

confidence: 99%

Section: Renal Lymphatic Physiology In Pathological Conditionsmentioning

confidence: 99%

Section: Renal Lymphatic Physiology In Pathological Conditionsmentioning

confidence: 99%

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Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

et al. 2019

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“…The presence of PC has already been linked to FD and reported in the literature as a possible feature of its renal involvement, but the etiology and exact mechanism of sinus cyst formation in FD remains to be elucidated [6][7][8][9][10][11][12][13][14][15][16]. A possible role of glycosphingolipid accumulation has been considered in the pathogenesis of human renal cystic diseases [17,18].…”

Section: Discussionmentioning

confidence: 99%

Novel Pathogenic Variant of Fabry Disease in a Family with Parapelvic Cysts

Greco,

Mollica,

Divilio

et al. 2023

J Biomed Res Environ Sci

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Background: Fabry's Disease (FD) is a rare, multi-organ lysosomal disease, caused by the deficiency of the enzyme α-galactosidase A. This leads to the accumulation of glycosphingolipids, particularly globotriaosylsphingosine (Lyso-Gb3), in visceral tissues and vascular endothelium throughout the body, with renal, cardiac, and central nervous system damage such that quality and expectancy of life are impaired. Progressive accumulation of Gb3 in podocytes, epithelial cells and the tubular cells of the distal tubule and loop of Henle contribute to the renal symptoms of Fabry disease, which manifest as proteinuria and reduced glomerular filtration rate leading to chronic kidney disease and progression to end-stage renal disease. We report the case of a patient with hypertension and proteinuria whose diagnosis of Fabry's disease was suspected due to the ultrasound finding of parapelvic cysts. Case presentation: A 41-year-old man with proteinuria and hypertension presented to our outpatient Department. The patient underwent a genetic investigation for Fabry due to the ultrasound finding of parapelvic cysts. We found a novel mutation c.160del in exon 1 of GLA gene with aminoacidic change in p. (Asp55ThrfsTer66). The new mutation was also found in the mother and his brother. In males, the elevated accumulation of LysoGB3 was associated with the presence of renal parapelvic cysts. Conclusion: This mutation is not reported in Fabry disease-associated mutation databases and has not been previously described in the literature but, the absent enzyme activity found in our patient, the significant blood accumulation of LysoGb3, as well as the type of mutation suggest its pathogenetic role. In addition, the novel mutation would appear to correlate with the occurrence of pelvic cysts in male subjects. Therefore Fabry’s disease should be suspected in male patients with hypertension, proteinuria and ultrasonographic finding of parapelvic cysts, especially in patients with otherwise unexplained cardiac, neurologic and/or ocular abnormalities. Further studies are needed to corroborate the finding.

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“…It is presently accepted that kidney lymphatics drain that organ's interstitial space (8,13). Renal lymph antibiotic levels have been the most successful method of estimating the actual tissue concentrations.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the Distribution of Tobramycin and Gentamicin in Body Fluids of Dogs

Szwed

Luft

Black

et al. 1974

Antimicrob Agents Chemother

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Tobramycin serum, thoracic lymph, renal lymph, and urine concentrations were measured in mongrel dogs after intravenously administered 5, 10, and 20 mg/kg doses. These were compared with intravenous gentamicin delivered at 5 and 20 mg/kg. Both drugs achieved similar concentrations in serum and thoracic lymph. At 20 mg/kg, tobramycin showed consistently higher renal lymph and urine concentrations than gentamicin. At 5 mg of tobramycin per kg, renal lymph and urine concentrations were higher than with gentamicin only within the 1st h after administration. Thereafter the difference was no longer significant. These data suggest that on the basis of distribution in the body fluids of dogs, tobramycin is a reasonable alternative to gentamicin.The clinical value of the aminoglycoside antibiotic, gentamicin, is undisputed. Its distribution in serum, urine, thoracic duct lymph, renal capsular lymph, and interstitial fluid has been well established, primarily through the work of Chisholm and Gingell and their co-workers (3,4,9,10). A new aminoglycoside, tobramycin, the sixth of eight antimicrobial factors produced by Streptomyces tenebrarius, is now available for investigation. This antibiotic is basically similar to gentamicin in structure, protein binding, and antibacterial spectrum (11,12,15,16,18,20). Studies suggest that it may be more effective against certain strains of pseudomonas and that it may manifest less ototoxicity than gentamicin (1, 2, 17). These characteristics would make tobramycin a welcome addition to the antibiotic armamentarium, especially if its distributional characteristics are the same as gentamicin. The present study was performed in order to measure and compare the rate of distribution and excretion of tobramycin and gentamicin in the body fluids of normal dogs. 15, 30, 45, 60, 180, 240, and 300 min. The specimens were analyzed for tobramycin or gentamicin by an agar well diffusion method by using Bacillus globigii as the test organism (14,19,21). Prior to analysis all urine specimens were buffered to pH 8 with phosphate buffers. Statistical studies consisted of computer-calculated means, standard errors, and an analysis of variance comparing the 5 and 20 mg/kg tobramycin and gentamicin groups, respectively. METHODS AND MATERIALS RESULTSThe distribution of tobramycin at 20, 10, and 5 mg/kg, as well as gentamicin at 20 and 5 mg/kg, in serum, thoracic lymph, renal lymph, and urine, is depicted in Fig. 1 to 4, respectively.The peak serum tobramycin concentrations ( Fig. 1)

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Summary of Renal Lymphatic Studies

Cited by 12 publications

References 6 publications

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

Renal Lymphatics: Anatomy, Physiology, and Clinical Implications

Novel Pathogenic Variant of Fabry Disease in a Family with Parapelvic Cysts

Comparison of the Distribution of Tobramycin and Gentamicin in Body Fluids of Dogs

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