In human nephrolithiasis, most stones are containing calcium and are located within urinary cavities; they may contain monohydrate calcium oxalate, dihydrate calcium oxalate and/or calcium phosphates in various proportion. Nephrolithiasis may also be associated with nephrocalcinosis, i.e., crystal depositions in tubular lumen and/or interstitium, an entity which suggests specific pathological processes. Several rodents models have been developed in order to study the pathophysiology of intrarenal crystal formation. We review here calcium rodent models classified upon the presence of nephrolithiasis and/or nephrocalcinosis. As rodents are not prone to nephrolithiasis, models require the induction of a long standing hypercalciuria or hyperoxaluria (thus explaining the very few studies reported), conversely to nephrocalcinosis which may occur within hours or days. Whereas a nephrotoxicity leading to tubular injury and regeneration appears as a critical event for crystal retention in nephrocalcinosis models, surprisingly very little is known about the physiopathology of crystal attachment to urothelium in nephrolithiasis. Creating new models of nephrolithiasis especially in different genetic mice strains appears an important challenge in order to unravel the early mechanisms of urinary stone formation in papilla and fornices. Core tip: We review here calcium rodent models classified upon the presence of nephrolithiasis or nephrocalcinosis which appear as two different entities. Nephrocalcinosis appears related to tubular cell injuries in the setting of urinary supersaturation whereas the pathophysiology of nephrolithiasis is mostly unraveled. Though few models are available, attachment of crystals in the fornix or in the MINIREVIEWS
Most mouse kidney stone models induce nephrocalcinosis rather than urolithiasis. The aim of our study was to find an accelerated experimental model in order to study the early events of stone formation, that is, at the time of crystal binding to intrarenal urothelium. C57B6 mice exposed to vitamin D supplements and water containing hydroxyl-L-proline, ammonium chloride and calcium chloride were studied for 42 days. A group receiving urothelial cell mitogen Fibroblast Growth Factor 7 (FGF7) was compared to control group receiving saline. Calcium oxalate monohydrate (COM) crystals were detected in urines by day 2 and within urinary spaces in specialized fornix areas in both groups as soon as day 14 with enhanced deposits in FGF7 group compared to controls at day 21. Urothelial cells proliferation, uroplakin III downregulation and de novo expression of osteopontin receptor CD44 detected in FGF7 group, were delayed in the control group (day 42). Crystal aggregates within specialized fornix areas by day 42 were located in urinary spaces but also within and under a multilayered metaplastic urothelium, simultaneous to macrophages influx. Point of note, administration of a normal diet by day 21 was responsible for a spontaneous crystal clearance. Our data show that under supersaturation conditions, urothelial cell proliferation and calcium oxalate crystal retention occur within specialized fornix areas. Enhanced crystal deposits following FGF7 administration suggest that urothelium proliferation would be a relevant trigger for renal stone formation.
Severe hypertension can lead to malignant hypertension (MH) with renal thrombotic microangiopathy and hemolysis. The role of plasma heme release in this setting is unknown. We aimed at evaluating the effect of a mild plasma heme increase by hemin administration in angiotensin II (AngII)-mediated hypertensive rats. Prevalence of MH and blood pressure values were similar in AngII and AngII + hemin groups. MH rats displayed a decreased renal blood flow (RBF), increased renal vascular resistances (RVR), and increased aorta and interlobar arteries remodeling with a severe renal microcirculation assessed by peritubular capillaries (PTC) rarefaction. Hemin-treated rats with or without AngII displayed also a decreased RBF and increased RVR explained only by PCT rarefaction. In AngII rats, RBF was similar to controls (with increased RVR). PTC density appeared strongly correlated to tubular damage score (rho = −0.65, p < 0.0001) and also renal Heme Oygenase-1 (HO-1) mRNA (rho = −0.67, p < 0.0001). HO-1 was expressed in PTC and renal tubules in MH rats, but only in PTC in other groups. In conclusion, though increased plasma heme does not play a role in triggering or aggravating MH, heme release appears as a relevant toxic mediator leading to renal impairment, primarily through PTC endothelial dysfunction rather than direct tubular toxicity.
Brief Communication Mycobacterium genavense is a non-tuberculous, slow-growing, acid-fast bacterium first reported in 1990. 7 This emerging opportunistic bacterium is responsible for disseminated diseases in immunocompromised human patients, 2 in many species of birds, 5 and in an increasing number of domestic animals including ferrets. 9,11,19 Fever, diarrhea, weakness, weight loss, hepatosplenomegaly, and lymphadenopathy are the usual clinical findings in humans and animals. Involvement of the lung, skin, and kidneys is also reported. 2,19 We report herein the postmortem, cytologic, and histopathologic description of disseminated M. genavense infection in a domestic ferret (Mustela putorius furo) in Europe. A 6-y-old male neutered ferret was presented with a 1-mo history of progressive weight loss, chronic cough, and hair loss. The cough had been treated with unspecified doses of sulfamethoxazole and prednisolone for 1 wk. The ferret was slightly depressed, hypothermic (rectal temperature of 36.2°C), had a body condition score of 2 of 5, and had bilateral serous epiphora. A dry "barking" cough was easily induced by tracheal palpation. A blood sample and radiographs were obtained under general anesthesia. The complete blood count was within normal reference intervals (RIs); serum biochemistry analysis revealed mild hypoglycemia (0.52 g/L; RI: 0.54-1.44 g/L). 6 Other biochemical parameters were within normal RIs. Radiographs showed multifocal peribronchial interstitial opacification throughout the lung, consistent with severe multifocal interstitial pneumonia. Abdominal ultrasound examination revealed a mass in the pancreaticoduodenal area. We suspected a pancreatic mass or pancreaticoduodenal lymphadenomegaly. Fine-needle aspiration of the pancreaticoduodenal mass was performed, and smears were stained with routine May-Grünwald/Giemsa (MGG). Cytologic examination revealed numerous epithelioid macrophages admixed with small lymphocytes and a few binucleate cells containing myriad intracytoplasmic, 2 × 0.5 µm, negative-staining rods. Subsequently, mycobacteriosis was highly suspected. One of the MGG-stained slides was dipped in alcohol until destained, and then restained with Ziehl-Neelsen (ZN) stain. Numerous 812137V DIXXX10.1177/1040638718812137Mycobacterium genavense in a domestic ferretDequéant et al.
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