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Biomedical subjects

K D Gardner

Publications and source records attributed to K D Gardner.

At least 73 records · Page 4Linked to original sources
PubMed1979

Nephron obstruction in nordihydroguaiaretic acid-induced renal cystic disease.

Studies were performed to characterize conditions in rat kidneys whose nephrons were made cystic by feeding 2% nordihydroguaiaretic acid (NDGA) to the animals. Using two micropipettes, we monitored intratubular hydrostatic pressures while perfusing single surface nephrons in NDGA-exposed (5 to 7 weeks) and normal rat kidneys. The introduction of 50 nl of Ringers solution labeled with 3H-inulin at a flow rate of 25 nl/min was associated with a significant mean (+/- SEM) increase (167 +/- 61%; P less than 0.02) in pressure in cystic but not in nondilated (-0.5 +/- 27.2%) or normal (31 +/- 23%) nephrons, respectively. The relative amount of 3H-inulin excreted in 40 min from cystic (4.0 +/- 2.0%) was less than that excreted from either nondilated (19 +/- 7%; P less than 0.05) or normal (105 +/- 26%; P less than 0.01) nephrons. Intralumenal pressures in nondilated but not other nephron groups correlated with urinary flow rates (r = 0.51; P less than 0.02). Single nephron filtration rates and tubular-fluid-to-plasma 3H-inulin rations in additional rats were similar among all groups of tubules. Concluding that these data reflected increased resistance to outflow from cystic nephrons, we examined these and additional NDGA-exposed (1 to 24 weeks) kidneys. 3H-thymidine radioautography demonstrated maximum collecting tubular cell hyperplasia (13% labeling) at 2 to 3 weeks of NDGA-exposure. Microscopy and microdissection demonstrated tiny mural polyps along outer medullary segments of collecting tubules. Thirteen tubules were traced to their outlets; polyps impinging on outflow lumens were found in all 13 instances. We conclude that partial nephron obstruction exists in NDGA-exposed kidneys and that obstruction is a likely contributor to cyst formation in this model.

Animals↗
PubMed1976

Gaps--anionic and osmolal.

Gaps is a bedside diagnostic game. It is played in two versions by nephrologists. It deserves wider application by the practicing physician. The more popular version, Anion Gaps, shows the presence of undetermined anions and alerts the physician to the possibilities of laboratory error, severe derangements in serum protein metabolism, or the ingestion of certain ionic compounds that directly or indirectly alter the concentration of routinely undetermined anions. A second version, Osmolal Gaps, shows the presence of unmeasured osmoles or of increased plasma solids and can be used in a variety of clinical situations to direct attention to laboratory, error, hyperproteinemia, hyperlipidemia, or the presence of unmeasured osmoles in the serum.

Acidosis, Respiratory↗
PubMed1976

Function and structure in the diphenylamine-exposed kidney.

Standard micropuncture and microdissection techniques were used to examine the function and structure of nephrons in rats whose kidneys were made cystic by dietary exposure to diphenylamine. Heterogeneity characterized the lesion, with dilation and frank cyst formation occurring in 5-30% of nephrons. Elevated intraluminal hydrostatic pressures, occurring in the absence of increased glomerular filtration or decreased net water reabsorption, were recorded in dilated, but not in nondilated nephrons. Structural studies demonstrated communication of dilated nephrons with cysts, concretions of debris within tubular lumens, evidence of extrinsic pressure by cysts on adjacent tubules, and apparent luminal narrowing of some proximal tubules. These observations were used to explain prolonged loop of Henle transit times and occasional failure to detect [3H]inulin excretion after microperfusion into dilated tubules. It was concluded that the elevated hydrostatic pressures in the dilated nephrons of diphenylamine-exposed kidneys were the consequence of variably severe and frequently incomplete tubular occlusion. These findings support the hypothesis that cyst formation is a consequence of partial obstruction and elevated intratubular pressure in this model and perhaps in other susceptible mammalian kidneys.

Aniline Compounds↗
PubMed1976

Hereditary renal-retinal dysplasia and the medullary cystic disease-nephronophthisis complex.

Nine of 81 members of two families were found to have renal problems. Three patients in one family had renal-retinal dysplasia with probable recessive inheritance. Of the 6 patients in the second family, one received a kidney transplant from his brother who initially had no detectable renal abnormality but later developed renal failure. In this family, the mode of inheritance seems to be dominant. Hereditary renal-retinal dysplasia differs from medullary cystic disease and nephronophthisis in its pattern of uniformly recessive inheritance and its accompaniment by retinitis pigmentosa. Because genetic considerations have important implications in selection of donors for renal transplant, these entities should be considered distinct despite the similarities in their clinical and pathologic features.

Adolescent↗
PubMed1976

Juvenile nephronophthisis and renal medullary cystic disease.

In the past 30 years 238 cases have been published which describe the nephronophthisiscystic renal medulla complex. Of these, 110 are sufficiently adequate to permit detailed analyses. Both isolated and genetically transmitted cases are reported. The latter include the dominant and recessive modalities, both autosomal, and the former perhaps also X-linked. Renal disease also has been inherited as a recessive trait in association with retinal degeneration. Medullary cysts have been found in 73% of cases in which kidney tissue has been examined directly. Their presence seems to bear no relationship to the ability of involved kidneys to conserve sodium. Salt wasting is described in the presence and absence of medullary cysts. Techniques short of anatomic examination of the kidneys have rarely allowed cysts to be detected and diagnosis continues to rest on a high index of suspicion, aroused in turn by a positive family history for the disease. Arterial hypertension occurs in roughly one third of cases. Aminoaciduria is not a part of the syndrome. A defect in maximum urinary concentrating ability may be the best single early sign of involvement but data are scarce.

Adult↗
PubMed1976

Comparison of human polycystic and medullary cystic kidney disease with diphenylamine-induced cystic disease.

Because of difficulty in obtaining cystic human kidneys for functional and morphologic study, animal models are receiving increasing attention. Most prominent among them is the renal cystic disease that is induced in rats through feeding of the antioxidant, diphenylamine, The present study examined the morphology of adult polycystic and medullary cystic kidney disease in man using scanning electron microscopy and compared them with diphenylamine-induced cystic kidney disease in rats. Diphenylamine nephropathy was induced by feeding rats 1 per cent diphenylamine for 12 to 18 months. All types of cystic disease showed changes in the renal corpuscles, including dilation of Bowman's space, podocyte fusion and degeneration, and basement membrane thickening. Cysts were noted along the entire nephron in polycystic and diphenylamine-induced cystic disease but only along the collecting ducts in medullary cystic disease. Cysts in polycystic disease were large and lined by flattened epithelium. Collecting duct cysts in diphenylamine cystic disease were lined by cells of irregular size and shape suggestive of cell hypertrophy and/or hyperplasia, whereas cysts of medullary cystic disease were lined by flattened epithelium except where the nephron entered or left the cyst. Cast material was generally found in the cysts of diphenylamine-induced and polycystic kidney disease but not medullary cystic disease. Atrophic glomeruli and tubules were found in all three diseases. Complete tubular obstruction was found in none; however, larger cysts frequently impinged on adjacent tubules and narrowed their lumina. The results of this study show that, in the terminal stages, cellular as well as gross morphologic differences exist between polycystic and medullary cystic kidney disease and that diphenylamine-induced cystic disease more closely resembles human polycystic than medullary cystic kidney disease.

Aniline Compounds↗
PubMed1975

Potassium. The intracellular cation.

Normally the concentration of potassium in the extracellular space is maintained within relatively narrow bounds; in disease, these boundaries may be exceeded. Hyperkalemia and sometimes hypokalemia must be considered medical emergencies, to be treated promptly, effectively, and appropriately.

Bicarbonates↗
PubMed1974

Cystic diseases of the kidney: a perspective on medullary cystic disease.

Fifty-two cases of adequately documented cystic disease of the renal medulla (CDRM) were selected from available literature and analyzed for hereditary mode, age at onset, and duration. In 17, recessively inherited disease appeared at 9.4+/- 1.6(SE) and lasted 7.2+/- 1.7 years while in 21, dominantly inherited disease appeared at 29.3 +/- 2.3 and lasted 2.4+/- 0.4 years. In 14 isolated cases similar data were intermediate. These findings support an hypothesis that at least two genotypes are responsible for the phenotypic expression of CDRM.

Adult↗