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The present article is reviewing the expressions of kidney disease emphasizing special precautions needed when treating these patients. For better life quality and prevention of life threatening complications.

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The present article is reviewing the expressions of kidney disease emphasizing special precautions needed when treating these patients. For better life quality and prevention of life threatening complications.

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Glomerulonephritis, particularly IgA nephropathy (IgAN), seems to be more common in familial Mediterranean fever (FMF), an inherited disease caused by mutations in the MEditerranean FeVer gene (MEFV). The present study is aimed to determine, in populations not suffering from FMF, whether carriage of MEFV mutations may modify or precipitate IgAN and other forms of primary glomerulonephritis (PGN). Forty patients with biopsy proven IgAN and 40 with PGN were surveyed for the presence of the three most common MEFV mutations (M694V, V726A and E148Q), using polymerase chain reaction amplification and restriction enzyme analysis. The rate of MEFV mutations in the patients was related to the expected carrier rate in the general population of the same ethnic extraction. The effect of mutation carriage on the disease course was determined in the IgAN patient group. The frequency of MEFV mutations in IgAN or PGN was comparable to that found in ethnically adjusted general population (p = 0.1 and 0.5, respectively). Carriage of mutated MEFV was not associated with the course and severity of the disease or findings in kidney biopsy and urine analysis. In a population, mostly of Jewish extraction, MEFV mutations do not seem to predispose to the development of IgAN and other forms of PGN or affect the phenotype.

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Mitochondrial DNA plays a crucial role in oxidative production of energy. Thus, defects in mitochondrial DNA can affect virtually all organ systems. The point mutation A --> G at position 3243 in the mitochondrial tRNAleu(UUR) gene is the cause of several distinct types of mitochondrial cytopathy and several clinical phenotypes, including encephalomyopathy with lactic acidosis and stroke-like episodes and maternally inherited diabetes and deafness. This mutation has been recently described also in association with kidney disease, mainly focal and segmental glomerulosclerosis. At present, little is known about the prevalence of this mitochondrial nephropathy, its clinical course and the pathogenesis of glomerular damage. We describe 2 unrelated patients, who presented with proteinuria and progressed to end-stage renal failure. Other clinical features were short stature, severe headache, hearing loss, diabetes mellitus and hypertrophic cardiomyopathy. The main histological finding was an increased number of abnormal mitochondria in tubular cells and podocytes. Analysis of mitochondrial DNA from leukocytes and urine sediment revealed heteroplasmy for the A3243G mutation in tRNAleu(UUR) gene in both patients. Recognition of the characteristic clinical and histological features of the mitochondrial A3243G mutation-associated glomerulopathy will enable correct diagnosis and better management of a disease which is likely to be underdiagnosed.

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OBJECTIVE: To report the case of a patient with manic-depressive disorder who developed lithium intoxcation following carbamazepine-induced acute renal failure. CASE SUMMARY: A 33-year-old white man with bipolar manic-depressive disorder was treated with lithium for the last 18 months. Three weeks prior to admission, carbamazepine 600 mg was added to the drug regimen due to a recurrence of the psychiatric disorder. He was admitted wh signs of lithium intoxication. Acute renal failure due to carbamazepine-induced interstitial nephritis was diagnosed. DISCUSSION: The combination of carbamazepine and lithium is known to cause neurotoxicity. We describe a different interaction in which the toxic lithium concentrations were the result of carbamazepine-induced acute renal failure. CONCLUSIONS: When considering adding carbamazepine to lithium, careful follow-up of the patients is warranted to prevent this indirect drug in interaction.

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Endogenous adenosine, secreted locally by the kidney during tissue hypoxia, induces heterogeneous renal hemodynamic responses. We investigated the cortical and outer medullary blood flow responses to intrarenal infusions of adenosine and adenosine A1- and A2-receptor agonists in anesthetized rats. These agents were infused into the renal interstitium through chronically implanted capsules, and blood flow was measured by laser-Doppler probes. Short (1 min, 0.05 ml) intrarenal infusions of adenosine (0.5 mumol) lowered cortical blood flow to 27 +/- 10% of baseline (n = 7, P < 0.0005). Medullary blood flow response was biphasic, i.e., a transient decrease in flow to 52 +/- 8% of baseline (n = 17, P < 0.0001) followed by a more-sustained increase in flow to 135 +/- 6% (n = 17, P < 0.0001). N6-cyclopentyladenosine, an adenosine receptor A1 agonist, reduced both cortical and medullary blood flow to 59 +/- 4% (n = 10, P < 0.0001) and 38 +/- 5% (n = 11, P < 0.0001) of baseline, respectively. By contrast, 2-[p- (carboxyethyl)phenethylamino]-5'-N-ethycarboxamidoadenosine (CGS-21680C), an adenosine receptor A2 agonist, increased dramatically the medullary blood flow to 184 +/- 15% of baseline (n = 12, P < 0.0005), without major changes in cortical flow. We conclude that intrarenal adenosine reduces cortical blood flow and predominantly increases medullary flow via A1 and A2 receptors, respectively. These hemodynamic responses could play a role in protection of the outer medulla from hypoxia.

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Patients with extensive atherosclerosis are at increased risk of developing embolic complications during cardiac catheterization. We describe a 51-year-old man with unstable angina and bilateral leg claudication who developed fever and right upper abdominal pain shortly after cardiac catheterization. Liver-spleen scintigraphy demonstrated a wedge-shaped filling defect compatible with splenic infarction, and serial scans performed over a period of five months showed resolution of this finding. Splenic infarction tends to be under-diagnosed, and physicians should be aware of this potentially serious complication of cardiac catheterization.

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Although generally a vasodilator, adenosine vasoconstricts cortical vessels in the kidney, reduces glomerular filtration rate (GFR), and increases medullary blood flow, effects likely to improve the medullary O2 deficiency characteristic of mammalian kidneys. To evaluate a possible role of adenosine in medullary O2 balance, we investigated the effect of adenosine upon cortical and medullary tissue PO2. Adenosine was infused into renal interstitium through chronically implanted capsules. Cortical and medullary PO2 were measured using sensitive Clark-type O2 microelectrodes inserted into kidneys of anesthetized rats at the respective depths of 1.8 and 3.7 mm. Infusion of adenosine (0.1-0.5 mumol/min) increased medullary PO2 from 17 +/- 3 (SE) to 40 +/- 5 mmHG (P less than 0.001) and decreased cortical PO2 from 64 +/- 4 to 47 +/- 3 mmHg (P less than 0.001). After the infusion was stopped, PO2 returned to baseline at both sites. Coadministration of adenosine receptor antagonist 8-phenyltheophylline (0.01 mumol/min) prevented both cortical and medullary effects of adenosine. We concluded that adenosine could play an important protective and regulatory role in renal medullary O2 balance.

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We investigated the role of the endothelial-derived relaxing factor nitric oxide (NO) in the homeostasis of O2 supply to the renal medulla, a region normally operating on the verge of hypoxia. Sensitive Clark-type O2 microelectrodes were inserted into renal cortex and medulla of anesthetized rats. The inhibitor of NO formation, L-NG-monomethylarginine (LNMMA), while increasing blood pressure and reducing renal blood flow, decreased medullary pO2 from 23 +/- 3 mmHg to 12 +/- 3 (P less than 0.001), with no change in the cortex. These responses were promptly reversed by L-arginine, which bypasses the LNMMA blockade. In isolated rat kidneys, LNMMA reduced perfusion flow without altering glomerular filtration rate, and augmented deep medullary hypoxic injury to thick ascending limbs from 68 to 90% of the tubules (P less than 0.02). These changes were prevented by L-arginine. Nitroprusside had a protective effect upon thick limb injury. Finally, in a previously reported model of radiocontrast nephropathy (1988. J. Clin. Invest. 82:401), LNMMA increased the severity of renal failure (final plasma creatinine from 2.3 +/- 2 mg% to 3.4 +/- 3, P less than 0.005) and the proportion of damaged thick limbs (from 24 +/- 6% to 53 +/- 9, P less than 0.01). Nitrovasodilatation may participate in the balance of renal medullary oxygenation and play an important role in the prevention of medullary hypoxic injury.

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The present report describes an unusual association between postpartum renal failure and systemic lupus erythematosus. Two healty young women developed progressive renal failure several weeks after delivery accompanied by the presence in their serum of strongly reactive anti-nuclear antibodies and positive anti-DNA antibodies. In both cases kidney biopsy disclosed light and electron microscopy pictures typical of idiopathic postpartum renal failure, with multiple intravascular thrombi and no evidence of active lupus nephritis. Intrarenal microthrombi formation may represent a form of exacerbation of systemic lupus erythematosus after delivery. The early recognition of this syndrome may have therapeutic implications.

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A 42-yr-old woman with familial dysautonomia (FD) presented with severe episodes of apnea during the daytime, as well as during sleep. Investigations revealed a megaesophagus and a lower esophageal constriction. These caused accumulation of food in the esophagus, resulting in recurrent aspiration and apnea which disappeared after gastrostomy. Megaesophagus, a rare complication in FD patients, can occur in other diseases with autonomic dysfunctions, and one must be aware of its potential respiratory complications.

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