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An unusual case of diarrhea.

The clue to this patient's correct diagnosis was his recent return from India. He usually visits there on an annual basis and the occurrence of posttravel infection has been noted in his medical records. This case study shows the importance of assessing patients for fever, abdominal cramps and diarrhea after recent travel outside of the United States. Shigella gastroenteritis should be in the differential diagnosis for patients with the above clinical presentation. The keys for diagnosis and prompt treatment of this disorder are to obtain the history, recognize symptoms, and order stool cultures.

Acute Disease↗

[Protection of rosiglitazone against renal interstitial lesion and its mechanism].

OBJECTIVE: To investigate the protection of rosiglitazone (RSG) against renal interstitial lesion and its mechanism. METHODS: Male adult SD rats were randomly divided into 5 groups: Sham group, undergoing sham operation; Sham + RSG group, undergoing sham operation and treated with RSG (30 mg.kg(-1).d(-1)); UUO group, undergoing unilateral left ureter obstruction; UUO + RSG5 group, undergoing UUO and treated with RSG (5 mg.kg(-1).d(-1)); and UUO + RSG30 group, undergoing UUO and treated with RSG (30 mg.kg(-1).d(-1)). Except the Sham group, the other groups were divided into 3 subgroups of 6 approximately 8 rats to be killed 3, 7, and 14 days after the intervention and their left kidneys were taken out to undergo light microscopy by Masson staining to observe the renal interstitial fibrosis index and to undergo immunohistochemistry with mice anti-rat ED-1 antibody to calculate the ED-1 (specific marker antigen on the surface of monocyte/macrophage) positive cells. Homogenate of renal cortex was made. ELISA was used to detect the protein expression of transforming growth factor beta(1) (TGF-beta(1)), bone morphogenetic protein (BMP)-7, and PAI-1 gene. RT-PCR was used to detect the mRNA expression of BMP-7 and TGF-beta(1) downstream effector genes: CTGF and Smad6. RESULTS: Fourteen days after the intervention, the fibrosis index of the UUO group were significantly increased and the fibrosis index values of both UUO + RSG5 and UUO + RSG30 groups were significantly lower than that of the UUO group (both P = 0.000) with a significant difference between the 2 UUO + RSG groups. Three days after the intervention, the number of ED-1 positive cell began to increase in the UUO group and peaked 7 days after, however, the number of ED-1 positive cells of the 2 UUO + RSG groups were significantly lower than that of the UUO group. TGF-beta(1) mRNA and protein were highly expressed in the UUO group, however, the expression of TGF-beta(1) mRNA in the 2 UUO + RSG groups was significantly lower, especially in the UUO + RSG30 group, in comparison with the UUO group (both P < 0.05). The CTGF mRNA expression was increased time-dependently in the UUO group, however the CTGF mRNA expression of the 2 UUO + RGS groups was significantly inhibited dose- and time-dependently (all P < 0.05). In comparison with that in the Sham group, the Smad6 mRNA expression was significantly increased in the Sham + RSG group (P < 0.05), and was decreased time-dependently in the UUO group; however, the decrease of Smad6 mRNA expression was significantly reversed in the 2 UUO + RSG groups, especially in the UUO + RSG30 group (P < 0.05). The expression of BMP-7 protein and mRNA was significantly lower in the UUO group time-dependently. However, the BMP-7 mRNA expression of the 2 UUO + RSG group, especially of the UUO + RSG30 group, was significantly higher than that of the UUO group (both P < 0.05). The PAI-1 protein expression of the UUO group was significantly higher 7 and 14 days after (both P < 0.05), however, the PAI-1 protein expression of the 2 UUO + RSG groups was significantly lower than that of the UUO group (both P < 0.05). CONCLUSION: RSG inhibits the renal interstitial macrophage infiltration, downregulates the expression of the down-stream target genes, and up-regulate the BMP-7 expression, thus blocking the renal fibrosis.

Animals↗

A progressive glomerulosclerosis occurring in partial five-sixths nephrectomized rats.

A chronic renal disease was induced by 5/6 nephrectomy in young adult Wistar albino male rats. Groups of 3 rats were killed at varying time intervals from 10 to 50 weeks after nephrectomy, and the glomerular structure was studied by light and electron microscopy. By light microscopy, increase in glomerular size and hypertrophy of the visceral glomerular epithelial cells were evident as early as the tenth week. Significant degree of glomerular hyalinization started on the 25th week and gradually became more extensive in involvement towards the 50th week. By electron miscroscopy, the hypertrophied glomerular epithelia showed many osmiophilic bodies and vacuoles in their cytoplasm and fusion of foot processes. Beginning on the 30th week, increase of the mesangial matrix was quite evident, and endothelial and epithelial cells disappeared from the areas where the increase was prominent. The increased matrix gradually encroached and occluded capillary lumina and Bowman's space, leading to a formation of obsolescent glomeruli. Whether or not these glomerular changes are due to the glomerular hyperfiltration which has been known to occur after 5/6 nephrectomy remains to be elucidated.

Animals↗

[Giant adrenal myelolipoma: hypertension, renal failure and spontaneous rupture].

Adrenal myelolipoma is a rare, benign, slow-growing tumor composed of adipose tissue and hematopoietic elements. It is usually diagnosed incidentally, although there are reports of patients with symptoms and descriptions of retroperitoneal hemorrhage due to rupture of large tumors. The condition has been associated with obesity, high blood pressure and adrenal dysfunction. We present a patient with retroperitoneal hemorrhage due to spontaneous rupture of a myelolipoma, hypertension, and renal failure secondary to nephroangiosclerosis.

Adrenal Gland Neoplasms↗

Recent perspectives in the mechanisms and therapy of renal sclerosis.

Chronic renal failure results from progressive sclerosis of injured kidney structures and overload of remnant functioning nephrons in an attempt to compensate for the lost excretory and fluid/solute regulatory capabilities. Key to delaying--or even reversing--the decay of renal function would be a therapy capable of blocking re-nal sclerosis. Therefore, a number of recent studies deal with this issue with a wealth of novel approaches. Considerable success has been achieved in experimental models by applying gene therapy, cell therapy, novel pharmacologic inhibitors of growth factors and matrigenic molecules. While the final step forward to human therapy is not an immediate option, it is likely that the next few years will witness initial trials of novel pharmacologic agents. Along with the already available new drugs suitable to prevent or delay renal transplant rejection or immunologic renal injury, the therapeutic scenario of contemporary nephrology is rapidly evolving. Some major novel findings in the area will be summarized, along with potential implications for human therapy.

Cell- and Tissue-Based Therapy↗

[P21 expression in renal interstitial fibrosis and regulative effect of enalapril].

OBJECTIVE: To investigate the expression of P21 in renal interstitial fibrosis rats and the effect of enalapril on it. METHODS: Sprague Dawley rats were randomly divided into 3 groups: a sham operation group,a unilateral urethral obstruction group, and an enalapril treatment group. The expression of P21 in renal tubular epithelial cells on the process was detected by immunohistochemistry at different time spots (7, 14, 21 d after UUO, sham-surgery or enalapril treatment). The expression of p21 mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Seven days after the surgery, significant differences were found in P21 expression between UUO and SOR renal tubular cells. With degree of interstitial fibrosis aggravating, P21 expression increased. Enalapril can inhibit its expression. CONCLUSION: In the kidney of UUO rats, P21 expression increased and enalapril possessed significant inhibitory effects on the procedure. P21 may participate in the pathogenesis of renal tubule-interstitial fibrosis.

Angiotensin-Converting Enzyme Inhibitors↗

[Expression of p27 in rat kidney with unilateral ureteral obstruction and the therapeutic effect of enalapril].

OBJECTIVE: To explore the effect of p27 in the renal tubule on the process of renal interstitial fibrosis caused by unilateral ureteral obstruction (UUO) in rats, and to examine the expression changes of p27 after enalapril intervention and to interpret the anti-fibrotic mechanism. METHODS: Ninety rats were randomly divided into the sham-operated group (SOR), UUO group,and UUO+enalapril treatment group [enalapril: 10 mg/(kg.d)]. The rats of each group were respectively sacrificed on 7, 14, 21 days post-operatively. The renal pathological changes were dynamically observed by HE. The expression and dynamic changes of p27 were detected by immunohistochemistry. The level of p27 mRNA were detected by RT-PCR. RESULTS: The expression of p27 in renal tubular epithelial cells and p27 mRNA were strongly positive in the SOR group. With degree of interstitial fibrosis aggravating, the expression of p27 mRNA was gradually reducing. Enalapril could improve the expression of p27 on the 14th and 21st days after the UUO. CONCLUSION: (1) This study supports a causative role of p27 in the formation of fibrosis of renal mesenchyme in rats with UUO. (2) The anti-fibrotic mechanism of enalapril is partly the improvement of p27 expression.

Angiotensin-Converting Enzyme Inhibitors↗

[Immunohistochemical study on the extracellular matrix components in various renal diseases].

In order to clarify considerable alterations of the extracellular matrix components in various renal diseases, monoclonal antibodies against type IV collagen (IV col), 200-KD laminin (200-KD Lam), 400-KD laminin (400-KD Lam) and heparan sulfate proteoglycan (HSPG) were applied to 142 renal biopsy specimens for the indirect immunofluorescence. These subjects included 5 cases with 1 hour specimen in the transplanted kidney, 32 minimal change nephrotic syndrome (MCNS), 30 mesangial proliferative glomerulonephritis (PGN), 2 focal segmental glomerulosclerosis (FGS), 21 membranous nephropathy (MN), 9 membranoproliferative glomerulonephritis (MPGN), 2 poststreptococcal acute glomerulonephritis (PSAGN), 13 diabetic nephropathy (DN), 16 lupus nephritis (LN), 9 diffuse sclerosing glomerulonephritis (DSGN), 2 amyloid kidney and 1 granulomatous nephropathy in sarcoidosis. In the transplanted kidney, the staining intensity of IV col was stronger than that of 200-KD Lam, 400-KD Lam and HSPG in general. IV col was predominantly distributed throughout the mesangium area and less along the glomerular basement membrane (GBM). The positive stainings with 200-KD Lam along the GBM and that with 400-KD Lam in the mesangium area were weakly recognized. HSPG was mainly detected along the GBM in the linear fashion. In MCNS, the distribution of the extracellular matrix components was mostly identical to that in the transplanted kidney. In the group of the glomerulonephritis showed the proliferations of mesangial cells, such as PGN and MPGN, the staining intensity of both IV col and 400-KD Lam, particularly in the latter, was remarkably increased in the sclerotic lesions. In MN, the thickened GBM was strongly stained with both IV col and 200-KD Lam, and the stainings of 200-KD Lam were more intensive. And still more, by the double labelling method performed for the couple of IV col and immunoglobulins, the correlation between glomerular capillary walls and/or mesangial areas and immunoglobulins deposits became more clear. These findings suggest as follows: (1) both IV col and 400-KD Lam, in particular 400-KD Lam, are possibly involved in the process of glomerulosclerosis: (2) both IV col and 200-KD Lam, in particular 200-KD Lam, are greatly involved in the process of new basement membrane-like materials formation in MN.

Collagen↗

[Acute oligoanuric renal insufficiency in malignant nephroangiosclerosis].

The concept of acute renal failure with anuria due to malignant nephro-angiosclerosis, is uncommon. We report two cases and compare them with others in the world literature. Knowledge of this disease entity is of triple interest: In diagnosis and classification in the field of acute vascular nephropathy with anuria. We cannot emphasise too much the interest of early renal biopsy after correction of abnormal blood pressure. In physiopathology, these malignant nephro-angioscleroses give rise to hypertension of pressor type with high renin levels. Finally therapeutic, for there exist drugs adapted to this type of hypertension. The association of acute renal failure and malignant nephro-angiosclerosis should be treated as an emergency, to avoid the passage to terminal and irreversible renal failure.

Acute Kidney Injury↗

National High Blood Pressure Education Program Working Group report on hypertension and chronic renal failure.

End-stage renal disease attributed to hypertension has increased annually for the last decade and will probably worsen through the year 2000. Patients with diabetic nephropathy and patients with hypertensive renal disease account for most new cases annually. Evidence reveals that all levels of untreated hypertension are associated with potentially declining renal function. Data from the Hypertension Detection and Follow-up Program and other studies show that antihypertensive treatment can prevent progressive renal failure. An ablation model demonstrates glomerular hyperfiltration as a possible mechanism for progressive renal failure. Human data on the renal effects of antihypertensive agents are limited and inconsistent. Despite the limitations, the Working Group on Hypertension and Chronic Renal Failure concludes that controlled hypertension to less than 140/90 mm Hg reduces the incidence of end-stage renal disease. Patients with established renal impairment may benefit from individualized treatment to 130/85 mm Hg or less.

Humans↗