scholarly journals II. RENAL THRESHOLD FOR HEMOGLOBIN IN DOGS UNINFLUENCED BY MERCURY POISONING

1932 ◽  
Vol 55 (4) ◽  
pp. 617-625 ◽  
Author(s):  
William H. Havill ◽  
John A. Lichty ◽  
Gordon B. Taylor ◽  
George H. Whipple
Keyword(s):  
Blood Plasma ◽  
Mercuric Chloride ◽  
Renal Injury ◽  
Active Part ◽  
Tubular Epithelium ◽  
Mercury Poisoning ◽  
Renal Threshold ◽  
Convoluted Tubules ◽  
Hemoglobin Threshold ◽  
Glomerular Tuft

The minimal or depression renal threshold for dog hemoglobin is not modified by moderate doses of mercuric chloride. This type of renal injury involves the epithelium of the convoluted tubules but the glomeruli escape. We are unable to explain our findings if we assume that the tubular epithelium takes an active part in the passage of dog hemoglobin from the blood into the urine. The evidence points toward the glomerular tuft as responsible for the passage of the hemoglobin from the blood plasma into the tubules. The glomerular tuft establishes the true hemoglobin threshold under these conditions. If the convoluted tubules are normal, we note that hemoglobin is taken into the epithelium and this explains the high initial renal threshold. With repeated hemoglobin injections this tubular epithelium becomes stuffed with hemoglobin pigment fractions and can absorb no more, which explains the minimal or depression threshold. Further injury of this tubular epithelium with mercury causes no change in this minimal renal threshold, unless we produce actual tubular obstruction.

scholarly journals IV. HEMOGLOBIN INJECTIONS AND CONSERVATION OF PIGMENT BY KIDNEY, LIVER AND SPLEEN

1932 ◽  
Vol 55 (4) ◽  
pp. 637-652 ◽  
Author(s):  
William V. Newman ◽  
George H. Whipple
Keyword(s):  
Threshold Level ◽  
Common Finding ◽  
Base Line ◽  
Staining Reaction ◽  
Renal Tubules ◽  
Tubular Epithelium ◽  
Renal Tubular Epithelium ◽  
Renal Threshold ◽  
Blood Hemoglobin ◽  
Convoluted Tubules

When the minimal renal threshold for blood hemoglobin is exceeded there is observed a deposit of iron staining pigment in the epithelium of the renal convoluted tubules. At a certain point this epithelium cannot take up more hemoglobin and this coincides with the minimal renal threshold level. When the injections of blood hemoglobin are kept below the minimal renal threshold level we note a complete absence of iron staining pigment in the renal tubular epithelium. Given a deposit of iron staining pigment in the tubular epithelium, it will slowly disappear during rest periods with no hemoglobin injections. Anemia due to bleeding will accelerate this removal of pigment from the renal epithelium and this indicates a conservation of material by the kidney for use in construction of new hemoglobin. Pigment giving a positive stain for iron will be found in the liver and spleen when hemoglobin injections are given, regardless of the renal threshold. Removal of this pigment is accelerated by anemia due to bleeding and as a rule an anemia period of 2 months at a level of 1/3 normal (40 to 50 per cent hemoglobin) will render the spleen, liver and kidney free from iron staining pigment. Pigment giving a positive iron stain is frequently observed in the mesenteric and lower retroperitoneal lymph glands. This is merely a drainage of pigment and phagocytes including pigment from some organ in which the pigment deposit was primary. In stock dogs in this laboratory the hemoglobin level is quite high when the animals are in a perfectly normal state. The blood hemoglobin averages 120 to 150 per cent hemoglobin. In such dogs iron staining pigment in the spleen is a common finding and on occasion is observed in the liver. To establish an accurate base line for the study of iron and iron staining pigment storage due to diet intake one must submit these dogs to a preliminary anemia period of at least 2 months. Muscle hemoglobin has a very low renal threshold and escapes freely into the urine when given intravenously. Contrasting with blood hemoglobin this musde hemoglobin under identical conditions does not cause the deposit of iron staining pigment within the epithelium of the renal tubules. A pigment giving no iron staining reaction may be found in the epithelium of the convoluted tubules of the kidney. Whether this is due to dietary or other factors is uncertain but this indicates pigment conservation by the kidney. Finally we would emphasize again the fact that the kidney is of considerable importance in the conservation of hemoglobin and hemoglobin split products which presumably are utilized to build up new hemoglobin.

Induction of heme oxygenase-1 in toxic renal injury: mercuric chloride-induced acute renal failure in rat

1998 ◽  
Vol 94 (1) ◽  
pp. 57-64 ◽  
Author(s):  
Saburo Horikawa ◽  
Koji Ito ◽  
Satoru Ikeda ◽  
Toshikazu Shibata ◽  
Shino Ishizuka ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Heme Oxygenase ◽  
Mercuric Chloride ◽  
Renal Injury ◽  
Heme Oxygenase 1

Acute Mercury Poisoning After Polyvinyl Alcohol Preservative Ingestion

PEDIATRICS ◽  
1980 ◽  
Vol 66 (1) ◽  
pp. 132-134
Author(s):  
James Seidel
Keyword(s):  
Aqueous Solution ◽  
Acetic Acid ◽  
Polyvinyl Alcohol ◽  
Mercuric Chloride ◽  
Medical Center ◽  
Mercury Poisoning

Polyvinyl alcohol preservative (PVA) is used routinely in the laboratory for collection of specimens for examination for ova and parasites.1-4 PVA, presently used at Harbor-UCLA Medical Center, contains: 4.5% mercuric chloride, 5% polyvinyl alcohol, 30% denatured alcohol, 4.5% acetic acid, and 1.5% glycerin in an aqueous solution. The kit, as shown in the Figure, contains three bottles with 10-ml aliquots of PVA, wooden sticks for mixing the specimen, and written instructions for collection of the specimens. The bottles are clearly labeled as poison in English and Spanish, and specific verbal as well as written instructions are given to patients and their families when the ova and parasite kits are dispensed.

Abstract 93: Hypertension and Renal Injury Induced by Nitric Oxide Depletion are Ameliorated by Concomitant Depletion of Hydrogen Sulfide

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Sebastiaan Wesseling ◽  
Joost O Fledderus ◽  
Johanna A Dijk ◽  
Chantal Tilburgs ◽  
Marianne C Verhaar ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Renal Injury ◽  
Renal Damage ◽  
No Synthase ◽  
Tubular Epithelium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Synthase Inhibitor

Chronic nitric oxide (NO) depletion induces hypertension and renal damage. Chronic kidney disease is associated with decreased NO availability and less renal H 2 S production. We hypothesized that combined depletion of NO and H 2 S aggravates hypertension and renal injury. Male 8-wk old Sprague Dawley rats were treated with vehicle, NO synthase inhibitor L-NG-nitroarginine (LNNA; 125 mg/L in drinking water), cystathionine-γ-lyase (CSE) inhibitor propargylglycine (PAG; 37.5 mg/kg BW ip daily) or LNNA + PAG for 1 and 4 weeks (6 rats/group). LNNA after 4w increased systolic blood pressure (SBP; 223±10 vs . 137±3 mmHg in controls; P<0.01), proteinuria (144±35 vs. 17±2 mg/d; P<0.01), uremia (16.6±4.2 vs . 7.0±0.4 mmol/L; P<0.05) and tubulo-interstitial injury (P<0.01). LNNA reduced urinary NO metabolite (NOx) excretion by ∼85% after 1w and 4w. PAG alone had no effect on SBP, renal function or injury, but did reduce urinary NOx excretion. Co-treatment with PAG ameliorated LNNA-induced hypertension (182±10 mmHg; P<0.01) and prevented proteinuria (27±3 mg/d), uremia (8.3±0.4 mmol/L) and tubulo-interstitial injury, but did not further reduce urinary NOx excretion. Renal H 2 S production was almost absent in all PAG groups after 1w and 4w (P<0.01) and was reduced in LNNA-treated rats after 4w (4.6±1.4 vs . 9.2±0.5 μmol/hr/mg; P<0.01). Renal HO-1 gene expression was strongly induced in all PAG-treated groups after 1w and 4w (4 to 19-fold; P<0.01) whereas LNNA only increased HO-1 gene expression at 4w (P<0.01). Immunohistochemistry showed that renal HO-1 protein was primarily interstitial in all PAG-treated groups at 1w and 4w. In contrast, LNNA only showed HO-1 in tubular epithelium in conjunction with protein casts. Depleting NO caused hypertension and renal damage followed by reduced renal H 2 S production and increased renal HO-1 expression. Surprisingly, concomitant inhibition of CSE ameliorated hypertension and prevented renal injury. PAG almost completely blocked renal H 2 S production and caused strong induction of renal HO-1, independently of injury, suggesting that H 2 S suppresses renal HO-1 expression. In conclusion, concomitant upregulation of HO-1 expression by inhibition of H 2 S production, prevents LNNA-induced hypertension and renal injury.

scholarly journals Acute Mercury Poisoning by Intentional Ingestion of Mercuric Chloride.

1997 ◽  
Vol 182 (4) ◽  
pp. 347-352 ◽  
Author(s):  
Minoru Yoshida ◽  
Hiroshi Satoh ◽  
Michirou Igarashi ◽  
Katsuya Akashi ◽  
Yukio Yamamura ◽  
...  
Keyword(s):  
Mercuric Chloride ◽  
Mercury Poisoning ◽  
Intentional Ingestion

scholarly journals MO1030THE FIRST CASE OF ATYPICAL HEMOLYTIC UREMIC SYNDROME (AHUS) FEATURES IN AN EXPERIMENTAL MODEL

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Guido Gembillo ◽  
Guido Bellinghieri ◽  
Vincenzo Savica ◽  
Rossella Siligato ◽  
Domenico Santoro
Keyword(s):  
Hemolytic Uremic Syndrome ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Rabbit Model ◽  
Acute Onset ◽  
Glomerular Lesion ◽  
First Case ◽  
Uremic Syndrome ◽  
Collecting Tubules ◽  
Convoluted Tubules ◽  
Glomerular Tuft

Abstract Background and Aims Thrombotic Microangiopathies (TM) are three distinct clinical syndromes presenting the same histological renal pattern: typical and atypical Hemolytic Uremic Syndrome (SEU- aSEU) and Thrombotic Thrombocytopenic Purpura (TTP). So far, the first report of a TM has been generally attributed to Eli Moschowitz. In 1922 he described the case of a 16 years old girl who died after acute onset of fever with petechial lesions and autoptic findings of hyaline thrombosis of terminal arterioles and capillaries, thus profiling the first case of TTP. Only in the 1955, Conrad Gasser described the first medical record of HUS, describing the case of a patient with a manifestation of bilateral necrosis of the renal cortex. We describe the first reported case of a Thrombotic Microangiopathy, in particular an experimentally induced aHUS by Richard M. Pearce in 1909. In this case, the trigger leading to aHUS was represented by snake venom injection in an experimental rabbit model. Method Pearce described acute glomerular lesions produced in the rabbit using dried venom of rattlesnake Crotalus Adamanteus. It was dissolved in salt solution in the proportion of 0.25 of a milligram to one cubic centimeter, rising gradually to two milligrams, and then followed by doses of 0.5 of a milligram of fresh venom at various intervals. The intervals between injections depended on the general condition of the animal and the amount of albuminuria. Results Rabbit kidneys showed well marked hemorrhagic and exudative lesions in the glomeruli; hyaline, granular, blood, and hemoglobin casts in both convoluted and collecting tubules; and granular degeneration of the epithelium of the convoluted tubules and loops of Henle. Pearce also described a “penetration of the cells of the compressed glomerular tuft into the mass of hemorrhage lying either in the tuft itself or in the capsular space” (Figure 1). In animals surviving 20-30 days after the first injection of the venom, the acute lesions were demonstrated to subside at the microscopic examination and their earlier presence was marked by “occasional casts and compressed masses of red cells in the glomerular spaces and tufts”. At the same time other models also showed “extensive granular degeneration of the convoluted tubules and many casts”. The renal autoptic findings presented the features of a vascular nephritis with severe endothelial changes. Conclusion Glomerular and tubular lesions of rabbits’ kidneys induced by crotalus’s venom showed typical features of what is today defined as aHUS. In this first experiment, the author described a glomerular tuft as “more analogous to the organization of a red thrombus than it is to any form of glomerular lesion known in man”, so we can affirm that Pearce described, ante litteram TMA histological features many years before other scientists.

scholarly journals A STUDY OF RENAL SECRETION DURING TARTRATE NEPHRITIS

1913 ◽  
Vol 18 (4) ◽  
pp. 347-352 ◽  
Author(s):  
Frank P. Underhill ◽  
H. Gideon Wells ◽  
Samuel Goldschmidt
Keyword(s):  
Sodium Chloride ◽  
Normal Animal ◽  
The Other ◽  
Tubular Epithelium ◽  
Histological Findings ◽  
Renal Secretion ◽  
Experimental Conditions ◽  
Convoluted Tubules ◽  
Intravenous Introduction ◽  
Direct Confirmation

After the intravenous introduction of a solution containing sodium chloride and urea into the rabbit during pronounced tartrate nephritis, all the chloride reappears in the urine within forty-eight hours. On the other hand, the nitrogen of the urine remains far below that usually eliminated by the normal animal under the experimental conditions; in other words, little or none of the urea injected is excreted by the kidney. In the light of the histological findings these results are interpreted to mean that under normal conditions chlorides and water are passed through the glomerular mechanism, whereas urea becomes a urinary constituent by way of the convoluted tubules. These results constitute a direct confirmation of the older observations of others concerning the elimination by the kidney of the substances under discussion. No evidence was obtained that the glomerulus may take over the function of the tubular epithelium.

Hepatocyte growth factor accelerates recovery from acute ischemic renal injury in rats

1994 ◽  
Vol 266 (1) ◽  
pp. F129-F134 ◽  
Author(s):  
S. B. Miller ◽  
D. R. Martin ◽  
J. Kissane ◽  
M. R. Hammerman
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Renal Injury ◽  
Artery Occlusion ◽  
Brdu Incorporation ◽  
Tubular Epithelium ◽  
Nitrogen Levels ◽  
Bilateral Renal Artery ◽  
Ischemic Renal Injury ◽  
Hepatocyte Growth

Effects of hepatocyte growth factor (HGF) administration were examined in a model of acute ischemic renal injury induced by bilateral renal artery occlusion in rats. Compared with rats administered vehicle, rats administered 20 micrograms HGF subcutaneously 30 min postischemia had significantly lower serum creatinine and blood urea nitrogen levels over the course of 7 days postocclusion, enhanced insulin clearances measured on day 2 postocclusion, reduced mortality, and much less injury evident by examination of kidney histologies 7 days postinjury. The tubular regeneration that occurred postischemic injury was reflected by increased incorporation of 5-bromo-2'-deoxyuridine (BrdU) in cortical tubular epithelium compared with incorporation in kidneys from noninjured rats. HGF enhanced BrdU incorporation compared with vehicle, indicating enhanced mitogenesis. The weight loss that occurs postischemic injury was not ameliorated by the dose of HGF we employed. We conclude that administration of HGF postischemic injury to rats stimulates the recovery of normal kidney function and the regeneration of proximal tubular epithelium.

scholarly journals Role of Some Natural Antioxidants in the Modulation of Some Proteins Expressions against Sodium Fluoride-Induced Renal Injury

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Ahlam M. Alhusaini ◽  
Laila M. Faddah ◽  
Naglaa F. El Orabi ◽  
Iman H. Hasan
Keyword(s):  
Dna Fragmentation ◽  
Sodium Fluoride ◽  
Renal Injury ◽  
Natural Antioxidants ◽  
Related Factor ◽  
Toll Like Receptor 4 ◽  
Altered Proteins ◽  
Vascular Adhesion ◽  
Convoluted Tubules

Background. The aim of the present work is to find the effects of N-acetylcysteine (NAC) and/or thymoquinone (THQ) in the protection against acute renal injury induced by sodium fluoride (NaF).Method. Rats were distributed into five groups: G1 was normal (control), G2 was intoxicated with 10mg/kg NaF i.p., G3 was treated with 10mg THQ /kg, G4 was treated with 20mg NAC /kg, and G5 was treated with a combination of THQ and NAC. The previous treatments were given daily along with NaF for four weeks orally.Result. Rats intoxicated with NaF showed a significant increase in serum urea, creatinine, uric acid, renal lipid peroxidation, nitric oxide, and TNF-αlevels, whereas the activity of superoxide dismutase (SOD) and glutathione (GSH) level was reduced. The expressions of Toll-like receptor-4 (TLR4), Lipocalin, vascular adhesion molecule-1(VCAM-1), and BAX proteins were upregulated, whereas Bcl-2 and NF-E2-related factor 2 (Nrf2) proteins expressions were downregulated. DNA fragmentation was also amplified. Histological analysis revealed that NaF caused a destructive renal cortex in the form of the glomerular corpuscle, the obliterated proximal and distal convoluted tubules, vacuolization in tubular cells focal necrosis, and cell infiltration. THQ and NAC supplementation counteracted NaF-induced nephrotoxicity as reflected by the increase in renal GSH and SOD. THQ and NAC ameliorated all the altered proteins expressions, improved renal architecture, and declined DNA fragmentation.Conclusion. The role of oxidative stress in the enhancement of NaF toxicity suggested the renoprotective effects of NAC and THQ against the toxicity of fluoride via multiple mechanisms.

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