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Biomedical subjects

K D Gardner

Publications and source records attributed to K D Gardner.

At least 19 recordsLinked to original sources
PubMed1997

Kidney and breast cysts: a comparative study of fluids.

The contributions of amino acids to the overall osmotic activity of cyst fluids were sought in this comparative study of fluids from the cysts of autosomal dominant polycystic disease (ADPKD) and gross cystic disease of the breast (GCDB). Fluids (n = 18) from 18 women with GCDB and from 8 patients with ADPKD (n = 25), grouped on the basis of sodium concentrations, were analyzed for potassium, chloride, protein, and osmolality by routine methods and for amino acids by reversed-phase high-pressure liquid chromatography. Similarities between kidney and breast cyst fluids included relative isosmolality, a wide range of sodium concentrations, an inverse relationship between sodium and potassium concentrations, higher concentrations of amino acids in low-sodium fluids, and significant correlations between sequential concentrations of amino acids in cyst fluids versus blood and some of its components. Therefore, cyst fluids in ADPKD and GCDB share compositional characteristics, and amino acids, possibly of blood protein origin, accumulate in small but osmotically significant amounts in some, particularly low-sodium, cysts of kidney and breast.

Amino Acids↗
PubMed1994

Cystic renal cell carcinoma and acquired renal cystic disease associated with consumption of chaparral tea: a case report.

Nordihydroguaiaretic acid is an antioxidant used experimentally to induce cystic renal disease in rats. It may be extracted from the leaves of the creosote bush, which are consumed as chaparral tea in the southwestern United States. We report a case of cystic renal disease and cystic adenocarcinoma of the kidney associated with a history of protracted consumption of chaparral tea.

Adenocarcinoma, Clear Cell↗
PubMed1994

Why renal cysts grow.

The growth of renal cysts leads to morbidity, contributes to mortality, and is a lesson in applied physiology. The fact that chemical, electrical, osmotic, and hydrostatic driving forces determine cyst volumes is inferred from observations that cyst fluids vary in their concentrations of osmotically active substances. Most have concentrations of sodium-based salts that are lower and nonsodium-based salts that are higher than those present in normal plasma. Nonsodium solutes include osmolytes that normally are present in higher concentrations inside of cells, including potassium, amino acids, and so-called idiogenic osmoles. The basic process of cyst growth therefore involves 1) the osmotic equilibration of water across cysts walls that have variable permeability characteristics and 2) the replacement of sodium salts with other osmotically active solutes in cyst fluids. Cyst volume is governed by the amounts and kinds of osmolytes that enter and become entrapped in lumina. Proliferation and necrosis of mural cells are events that are fundamental to the growth of renal cysts.

Animals↗
PubMed1993

Hyperplasia and fluid accumulation in epithelial cyst formation and growth.

Epithelial cysts may develop in virtually any epithelium. All cysts, regardless of their origins, are characterized by epithelial hyperplasia and fluid accumulation. Additional features may include tubular atrophy, basement membrane alterations and association with inflammatory cells. In spite of the intense research effort in recent years directed at uncovering the cellular mechanisms of cyst development and growth, we still do not know the primary events that lead to cyst formation. However, there are at least three candidate mechanisms. These include: 1) increased cell proliferation (epithelial hyperplasia) in the cyst wall, 2) net fluid accumulation in the cyst cavity and 3) alterations of extracellular matrix components linked to cyst formation and growth. This review discusses the evidence to support the role of each mechanism as a possible primary event necessary for cyst initiation and continued enlargement. Present data on the pathogenesis of epithelial cyst formation strongly suggests that no single mechanism, as yet described, can adequately account for all situations of cyst occurrence.

Animals↗
PubMed1992

On the probability that kidneys are different in autosomal dominant polycystic disease.

We hypothesized that highly variable cyst fluid sodium concentrations are a characteristic of every kidney in autosomal dominant polycystic kidney disease (ADPKD). We added our data on sodium concentrations in 124 fluids from ten ADPKD kidneys to data published by others of concentrations in 32 fluids from five kidneys. The values ranged from 3 to 207 mEq/liter; none fell between 59 and 74 mEq/liter. Fluids were designated as low (< 60 mEq/liter; 50 fluids) or high (> 60 mEq/liter; 106 fluids) sodium fluids. Transmission electron microscopy identified differences in the depths of apical tight junctions between cells from cyst walls of 12 of the low and 10 of the high sodium fluids from two kidneys (mean +/- SE depths of 2039 +/- 74 A vs. 386 +/- 18 A respectively; P < 0.0001). When fluids were grouped by kidney of origin, six of the 15 kidneys had only high sodium fluids. The probability that chance had led to the sampling of only high sodium fluids in these organs, given that 32% of all fluids were low sodium fluids, was calculated at < 0.00015. The possibility must be considered that all kidneys are not alike in ADPKD.

Adult↗
PubMed1992

Phenotype recognition. Clinicians' contributions to molecular genetics.

Medullary cystic disease, Alport's syndrome, and autosomal dominant polycystic kidney disease are inherited renal disorders whose genetic bases are better understood because of careful clinical observation. I explore the relationships among some clinical aspects of each of these conditions, the rapidly advancing field of molecular genetics, and the ethical issues that need to be addressed before gene identification becomes too widely applied as a diagnostic tool.

Ethics, Medical↗
PubMed1991

Cytokines in fluids from polycystic kidneys.

We sought evidence of cytokine presence and interleukin-1 beta (IL-1 beta) bioactivity in 104 aerobic culture negative cyst fluids (CFs) from 13 kidneys of 13 patients with symptomatic normal to end-stage autosomal dominant polycystic kidney disease (ADPKD). ELISAs were used to detect IL-1 beta, interleukin-2 (IL-2), tumor necrosis factor alpha (TNF alpha) and stromelysin. Prostaglandin E2 (PGE2) was detected by radioimmunoassay. IL-1 beta was present in 65 of 94 (less than 20 to 419 pg/ml, TNF alpha in 54 of 75 (less than 10 to 73 pg/ml), stromelysin in 18 of 23 (less than 1.0 to 56 ng/ml), IL-2 in 7 of 23 (0.1 to 1.3 ng/ml) and PGE2 in 9 of 10 fluids (0.03 to 0.49 ng/ml). Of 51 fluids with immunoreactive IL-1 beta, 36 were mitogenic for thymocytes. IL-1 beta concentrations correlated directly with those of IL-2; IL-1 beta presence was associated with higher stimulation indices, higher mean concentrations of TNF alpha, IL-2, stromelysin, and PGE2, and with positive endotoxin assays, suggesting activation of the cytokine cascade in vivo. Cytokine, stromelysin and PGE2 concentrations did not correlate with sodium or non-sodium solute concentrations, nor with CF blood, osmolality, or endotoxin activity, indicating that differences in concentrations among fluids could not be explained by differences in water content. These data identify cytokines as candidate contributors to the morbidity and pathogenesis of ADPKD.

Adult↗