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Acute Toxic Nephropathies: Clinical Pathologic Correlations - ROBERT C ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 6, No. 6 Copyright © 1976, Institute for Clinical Science Acute Toxic Nephropathies: Clinical Pathologic Correlations - ROBERT C. MUEHRCKE, M.D.,* FREDERICK I. VOLINI, M.D.,f ARTHUR M. MORRIS, M.D.,f JOSEPH B. MOLES, M.D.,f and ARTHUR G. LAWRENCE, M.D.,f *West Suburban Kidney Center and fWest Suburban Hospital, Oak Park, IL 60302 ABSTRACT Man’s ever increasing exposure to numerous drugs and chemicals, which are the results of medical and industrial progress, produces a by-product of acute toxic nephropathies. These include acute toxic renal failure, drug- induced acute oliguric renal failure, acute hemorrhagic glomerulonephritis, nephrotic syndrome, tubular disturbances and potassium deficiency. In depth information is provided for the previously mentioned disorders. Introduction have extremely vascular renal medullae Acute toxic nephropathy is a by­ and rete mirabile that function in the product of man’s ever increasing expo­ final dilution and concentration of the sure to a vast array of various chemicals urine. This complex mechanism results and drugs that result from industrial and in hypertonicity of the renal interstitium medical progress. The kidney, with its with concentration of nephrotoxic chemi­ rich blood supply, numerous enzyme sys­ cals, biologic products and drugs. tems and superior excretory function, is In our experience, approximately 25 especially vulnerable to the adverse ef­ percent of all patients with acute oliguria fects of chemicals, biologic products and have renal failure induced by drugs or drugs.44,226 The kidneys comprise 0.4 chem icals.188 The other main clinical percent of the total body weight and re­ syndrome of toxic nephropathy include quire a high oxygen consumption. The the nephrotic syndrome,133,180,256 tubular kidney’s oxygen required is supplied d iso rd ers,96 acute hemorrhagic through approximately 20 to 25 percent of glomerulonephritis and chronic renal the cardiac output. failure. Although the kidneys are of relatively small weight, they have the greatest sur­ M echanism face area of endothelial cells when com­ Nephrotoxic chemicals have exerted pared to other organs. The kidneys with these adverse effects on the kidney either their numerous enzyme system are sec­ singly or through a combination of ond only to the liver in complexity of pathopharmacologic mechanisms. One metabolic function. Finally, the kidneys mechanism is the direct action of the 4 7 8 MUEHRCKE, VOLINI, MORRIS, MOLES AND LAWRENCE nephrotoxic substance as a protoplasmic the nephrotoxic effect of meralluride poison. The nephrotoxic agent passes (Mercuhydrin), which reacts with en­ into the glomerular filtration in an zyme systems of the sulfhydryl groups amount proportionate to the filtered within the wall of mitochondria. Other plasma water. As the nephrotoxic sub­ nephrotoxins couple with enzymes to in­ stance is a foreign compound and has no activate them. Some nephrotoxins affect specific renal tubular transport process, it enzymes within the mitochondria, while is progressively concentrated within the other toxins affect cytoplasmic enzymes. tubular lumen. The concentration of the This functional interference may result in nephrotoxic agent is so great that it dam­ no apparent tubular morphologic abnor­ ages the tubular epithelial cells. malities when the tissue is studied by Moreover, other nephrotoxic substan­ light or electron microscopy. Other pro­ ces204,228,238 may increase in their concen­ toplasmic toxins, when concentrated, tration to reach toxic levels within the may coagulate protein and may result in medullary interstitium by the osmotic either severe tubular necrosis or diffuse concentration of fluids. When sufficient bilateral renal cortical necrosis. quantity is accumulated, the kidney in­ O ther nephrotoxic agents produce their terstitium is damaged. Chronic phenace- adverse effects through an immunologi­ tin nephritis is one example of such a cal pathopharmacologic mechanism. The condition.103,147,224 best example of such a model is duck egg Some nephrotoxic substances penetrate albumin. The morphologic site involved the cell to interact with cellular con­ is usually the large endothelial surface of stituents and, subsequently, poison the the glomerular capillaries, arterioles and cell. One example of this mechanism is arteries. The duck egg albumin acts as an antigen evoking a production of antibody. T A BLE I Immune complexes formed in the pres­ Common Chemicals that Induce ence of complement produce damage to Acute Oliguric Renal Failure glomerular capillaries. Mean Lethal Dosage Another important additional site in­ (Approximately Chemical per 70 kg) volved by hypersensitivity reactions is the renal interstitium. This hypersen­ Anilin 10 g sitivity interstitial reaction was reported Arsine gas (AsH-j) MAC* 30 ppm Camphor 2 g more than 75 years ago by Councilman.60 Carbon tetrachloride 4 ml (MAC* 25 ppm) Known as “Councilman’s interstitial Chlordane 8 g Chloroform 25 ml nephritis,” it is characterized by intersti­ Copper compounds 15 g tial infiltrates of plasma cells, small lym­ Creosote 10 g Essential (volatile) oils 1 9 phocytes, and eosinophils. A few of the Ethylene dischloride MAC* 100 ppm Ethylene glycol 100 ml drugs that cause this hypersensitivity Formaldehyde (formalin) 30 ml reaction are phenindione, diphenylhy- Guaiacol 2 9 -a Mercury compounds MAC* 0.1 mg/MJ dantoin (Dilantin), methicillin, phenyl­ i g butazone and meralluride (Mercuhyd­ Naphthalene 5 g Oxalates 5 g rin). Paradichlorobenzene 15 g Pentachlorophenol i g In general, substances toxic to the kid­ phenol 10 g Phosphorus, yellow 0.05 g (MAC* 1 g/M3) ney include chemicals, as presented in Resorcinol 2 g table I, in any physical state (liquids, sol­ Tetrachloroethane. MAC* 5 ppm ids, and gases); biologic products such as Thymol 2 g horse serum, fungi (mushrooms), and *MAC - maximum allowable concentration vaccines; and drugs given orally or par­ ACUTE TOXIC NEPHROPATHIES 479 enterally. Drugs produce other clinical treatm ent.138, 167,169 Six patients were syndromes of renal disease, including the treated after uremia occurred, and only nephrotic syndrome, chronic renal fail­ three of those six survived.168 BAL ap­ ure, tubular disturbances and acute pears to enhance the removal of mercuric hemorrhagic glomerulonephritis. In ions by 7 to 11 percent with the use of some situations, the damage is mild and hemodialysis.15 transitory. In other situations, the damage The clinical symptoms of inorganic is severe and irreversible leading to the mercury poisoning begin with a lingering patient’s death. bitter and metallic taste in the mouth. The patient experiences a sensation of throat constriction, suffocation, subster- Acute (Toxic) Renal Failure nal burning, gastritis, abdominal pain The more common nephrotoxins pro­ and, finally, nausea and vomiting.109 Per­ ducing acute renal failure are heavy met­ sistent vomiting leads to retching of als, organic solvents, glycols, analine, in­ blood. Ulceration may be noted in the pa­ secticides, arsine, cresol and a miscel­ late. The patient goes into circulatory laneous group of chemicals. They usually failure; the pulse becomes weak and act directly on the tubular cells to disrupt rapid. Syncope and shock are followed by their metabolic and morphologic integ­ a scanty urinary output. Finally, a fatal rity. anuria develops. Jaundice occurs in ap­ proximately 35 percent of the patients. M e r c u r y C o m p o u n d s The kidneys of patients with inorganic mercury poisoning are usually enlarged The inorganic salt bichloride of mer­ and weigh up to 250 g each. The renal cury (mercuric chloride) is also known as cortex is pale and thickened. The renal corrosive sublimate. Mercuric chloride is medullae are a slightly darker brown than usually ingested accidentally,175 in suici­ normal. The most striking morphologic dal attempts,34 or following its use as an abnormalities occur in the proximal con­ abortive agent. The dose required to in­ voluted tubules.97 There is extensive cel­ duce renal failure is difficult to assess.71 lular necrosis and the lumina are filled In most reports the patients with acute with granular eosinophilic material be­ renal failure had ingested two or three lieved to be derived from the cytoplasm tablets (0.5 g each).129 When more than of necrotic cells.61 Less striking abnor­ four tablets were taken, acute oliguric malities are found in the ascending renal failure was fatal. Renal lesions de­ limbs, distal convoluted tubules and col­ veloped within three hours after inges­ lecting tubules. In approximately one tion.47,245 Emetic and gastric lavage so­ week, the luminal necrotic debris clears, lutions can be made from a glass of probably because of digestion by plas­ skimmed milk with three to four tea­ mo lytic enzymes. In addition, the debris spoons of table sugar, two tablespoons is washed down the nephron lumen by of baking soda and three eggs. the glomerular filtrate. The proximal Schreiner and Maher described 11 pa­ tubule appears to be dilated and lined by tients who had mercuric chloride- flat epithelial cells.181 Patchy calcification induced acute oliguric renal failure.225,223 may occur in severely damaged tubules. Five patients who survived were treated Interstitial edema is noted early; if within 48 hours after ingesting mercuric oliguria is prolonged, interstitial fibrosis chloride; hemodialysis and dimercaprol ensues. Mercurials have produced the (BAL) infusion were the methods of nephrotic syndrome in some patients.17 4 8 0 MUEHRCKE, VOLINI, MORRIS, MOLES AND LAWRENCE C a r b o n T etrachloride The onset of oliguria is prolonged and Carbon tetrachloride (CC14) is widely may occur seven to ten days after expo­ used as an industrial solvent, as a house­ sure. Some patients may have forgotten hold cleaning agent, as a constituent in their exposure to this solvent. Absolute certain types of fire extinguishers, in some anuria may last from one day to several hair lotions, as an antihelmintic agent and weeks. One patient had carbon as a vermifuge.2 It is a volatile, heavier tetrachloride-induced oliguria for 67 days.
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