Biomedical subjects

Maria Picken

Publications and source records attributed to Maria Picken.

7 recordsLinked to original sources

PubMed2006

Spontaneously reduced blood pressure load in the rat streptozotocin-induced diabetes model: potential pathogenetic relevance.

The rat streptozotocin (STZ)-induced diabetes model is widely used to investigate the pathogenesis of diabetic nephropathy. However, overt nephropathy is inexplicably slow to develop in this model compared with renal mass reduction (RMR) models. To examine whether blood pressure (BP) differences correlated with the time course of glomerulosclerosis (GS), BP was measured continuously throughout the course by radiotelemetry in control (n = 17), partially insulin-treated STZ-diabetes (average blood glucose 364 +/- 15 mg/dl; n = 15), and two normotensive RMR models (systolic BP <140 mmHg)--uninephrectomy (UNX; n = 16) and 3/4 RMR by surgical excision [right nephrectomy + excision of both poles of left kidney (RK-NX); n = 12] in Sprague-Dawley rats. Proteinuria and GS were assessed at approximately 16-20 wk (all groups) and at 36-40 wk (all groups except RK-NX). At 16 wk, significantly greater proteinuria and GS had developed in the RK-NX group compared with the other three groups (not different from each other). By 36-40 wk, substantial proteinuria and GS had also developed in the UNX group, but both the control and the STZ-diabetic rats exhibited comparable modest proteinuria and minimal GS. Systolic BP (mmHg) was significantly reduced in the STZ-diabetic rats (116 +/- 1.1) compared with both control (124 +/- 1.0) and RMR (128 +/- 1.2 and 130 +/- 3.0) groups (P < 0.01). Similarly, "BP load" as estimated by BP power spectral analysis was also lower in the STZ-diabetic rats. Given the known protective effects of BP reductions on the progression of diabetic nephropathy, it is likely that this spontaneous reduction in ambient BP contributes to the slow development of GS in the STZ-diabetes model compared with the normotensive RMR models.

Animals↗

PubMed2006

Fat poor renal angiomyolipoma: patient, computerized tomography and histological findings.

PURPOSE: We reviewed our experience with fat poor cases of angiomyolipoma. MATERIALS AND METHODS: The records of patients with angiomyolipoma, as determined by pathological study, from 1998 to 2004 were reviewed by recording patient demographics and outcomes. Fat poor cases were defined as the failure of imaging to demonstrate fat in a lesion. Computerized tomography and histological characteristics were assessed. RESULTS: Histologically confirmed angiomyolipoma was found in 15 patients. Multiple lesions were found in 3 of 15 cases (20%). Of these 15 patients who underwent surgery 11 (73%) had unsuspected angiomyolipoma due to absent fat on computerized tomography and they underwent intervention for presumed renal cell carcinoma. Mean age +/- SD in this group was 54 +/- 15 years and 8 of 11 patients (73%) were female, of whom 4 (50%) had uterine fibroids. These lesions were found incidentally in 7 of 11 cases (64%). Operative complications developed in 2 of 11 patients (18%). Average maximal diameter on pathological evaluation was 3.2 +/- 1.3 cm (range 1.5 to 6). Nonenhanced computerized tomography was available in 7 of 11 cases, of which 3 of 7 (42%) showed hyperdense lesions and 4 of 7 (57%) showed isodense lesions. The percent of fat identified per high power field was less than 25% in 12 of 13 fat poor angiomyolipoma lesions (92%) compared to 2 of 4 classic lesions (50%) known to be angiomyolipoma before surgery (p = 0.04). CONCLUSIONS: We suggest that a general definition of fat poor angiomyolipoma should be the failure of imaging to reveal fat within a lesion, thus, making it unsuspected at surgery. A pathological definition should be less than 25% fat per high power field, which to our knowledge is a formerly undefined quantity. Not all cases are hyperdense on nonenhanced computerized tomography. These lesions cannot be reliably identified by imaging and they should be managed like all enhancing renal masses.

Adipose Tissue↗

PubMed2004

Heart transplantation in a patient with chloroquine-induced cardiomyopathy.

We present the first report of a patient who underwent heart transplantation (HT) after endomyocardial biopsy (EMB) and revealed chloroquine-induced cardiomyopathy (CIC). This patient, who was treated with chloroquine for 6 years, developed a restrictive cardiomyopathy that progressed to congestive heart failure (CHF) resistant to medical management.

Antirheumatic Agents↗

PubMed2003

Low protein diet mediated renoprotection in remnant kidneys: Renal autoregulatory versus hypertrophic mechanisms.

BACKGROUND: The mechanism of low protein diet conferred renoprotection in the ablation model remains controversial. Blockade of glomerular hypertrophy, reduced preglomerular vasodilation, and preserved autoregulation have all been postulated. The potential differential impact of calcium channel blockers on these mechanisms and glomerulosclerosis was examined. METHODS: Rats with 5/6 renal ablation received either a 25% standard protein diet, an 8% low protein diet and a low protein diet with either verapamil or amlodipine. Renal autoregulatory and morphometric studies were performed at 3 weeks before the development of significant injury, and the assessment of glomerulosclerosis after 7 weeks of continuous blood pressure radiotelemetry in additional rats. RESULTS: The preserved renal autoregulation in low protein rats was abolished by both calcium channel blockers, with the impairment being either comparable to (low protein + verapamil) or greater than the standard protein rats (low protein + amlodipine). Neither calcium channel blocker blocked the inhibitory effects of low protein diet on renal blood flow, kidney weight, and glomerular volume. Results (mean +/- SE) for glomerular volume (microm-3x 10(-6)): low protein (N = 11), 1.6 +/- 0.1; low protein + verapamil (N = 10), 1.7 +/- 0.1; low protein + amlodipine (N = 12), 1.7 +/- 0.2; versus standard protein (N = 10), 2.2 +/- 0.1; P < 0.05. Only amlodipine, but not verapamil, reduced average systolic blood pressure (143 +/- 2 mm Hg versus low protein rats, 168 +/- 5 mm Hg, and standard rats, 170 +/- 6 mm Hg; P < 0.01). Nevertheless, the glomeruloprotection seen in low protein (N = 15) as compared to standard protein (N = 14) rats (9%+/- 3% versus 28%+/- 6% glomerulosclerosis; P < 0.01) was abolished in both low protein + verapamil (N = 14, 32%+/- 7%) and low protein + amlodipine rats (N = 16, 27%+/- 7%). CONCLUSIONS: Preservation of renal autoregulation and not inhibition of hypertrophy is the critical component in low protein diet-conferred glomeruloprotection.

Amlodipine↗

PubMed2003

Comparison of laparoscopy-assisted partial nephrectomy using digital compression versus purely laparoscopic nephrectomy using vascular pedicle clamp in a porcine model.

BACKGROUND AND PURPOSE: Laparoscopic partial nephrectomy raises a number of technical issues, particularly in the control of bleeding. We compared digital compression during hand assistance with a vascular clamp. MATERIALS AND METHODS: Laparoscopic transperitoneal bilateral lower-pole partial nephrectomy was performed on six pigs, with a vascular clamp being used on one side and digital pressure through an Omniport or Lapdisk on the other. The pigs were then euthanized and the kidneys harvested for histologic examination. RESULTS: Good hemostasis was obtained regardless of the technique. However, the estimated blood loss was significantly greater with digital compression (96.7 versus 9.6 mL). There were no significant micropathological differences in the kidneys. The surgeons rated suture tying and placement much easier with the purely laparoscopic technique. CONCLUSIONS: Both techniques are feasible. In experienced hands, the purely laparoscopic technique takes no longer than the hand-assisted technique and is associated with less blood loss, easier suturing, and better cosmesis. However, long-term follow-up is needed before clinical use can be contemplated.

Animals↗

PubMed2003

Renoprotection by ACE inhibition or aldosterone blockade is blood pressure-dependent.

Renin-angiotensin-aldosterone system blockade has been shown to protect against renal damage in salt-supplemented, stroke-prone spontaneously hypertensive rats (SHRsp). Based on intermittent tail-cuff blood pressure (BP) measurements, it has been claimed that such protection is BP-independent and mediated by a blockade of the direct tissue-damaging effects of angiotensin and/or aldosterone. BP radiotelemetry was performed for 8 weeks in approximately 10-week-old male SHRsp who received a standard diet and either tap water (n=10) or 1% NaCl to drink. Saline-drinking SHRsp were either left untreated (n=12), received enalapril (50 mg/L) in drinking fluid (n=9), or had subcutaneous implantation of time-release 200-mg pellets of aldactone (n=10). The average systolic BP (mean+/-SEM) during the final 3 weeks was significantly higher (P<0.05) in untreated saline-drinking (215+/-6 mm Hg) SHRsp but not aldactone-treated (198+/-4 mm Hg) or enalapril-treated treated SHRsp (173+/-1 mm Hg), as compared with tap water-drinking SHRsp (197+/-3 mm Hg). Histological renal damage scores at 8 weeks paralleled the BP in all groups, with an excellent correlation (r=0.8, P<0.001, n=41). Moreover, a renal damage score of >5 was only observed in SHRsp whose average systolic BP during the final 3 weeks exceeded 200 mm Hg, indicating a threshold relation with BP. These data show that protection by renin-angiotensin-aldosterone system blockade in this model is BP-dependent and mediated by preventing the severe increases in BP seen in untreated salt-supplemented SHRsp and further underscore the limitations of interpretations based on conventional tail-cuff BP measurements.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2002

Increased genetic susceptibility to renal damage in the stroke-prone spontaneously hypertensive rat.

BACKGROUND: The spontaneously hypertensive rat (SHR) develops much less renal damage than the stroke-prone strain of SHR (SHRsp) after salt-supplementation, and it has been proposed that these strains differ in their genetic susceptibility to renal damage. However, radiotelemetric BP measurements have shown that salt-supplementation results in more severe and accelerated hypertension in the SHRsp. Therefore, it is unclear whether the differences in renal damage are due to differences in BP exposure or true differences in intrinsic (genetic) renal susceptibility to hypertensive damage. METHODS: Kidney cross transplantation was performed between the SHR and SHRsp strains in uninephrectomized recipients to allow an investigation of the susceptibility to renal damage in SHR and SHRsp kidneys maintained in the same host and exposed to the same BP profile and metabolic environment. Following transplantation, BP was radiotelemetrically monitored before and after an 8% NaCl diet given to accelerate hypertension and renal damage. Then the kidneys were removed and renal damage was assessed histologically. RESULTS: In the SHR recipients, the SHRsp donor kidneys exhibited more hypertensive damage than the contralateral native SHR kidneys, but histologic evidence of mild cellular immunologic rejection also was observed that could have facilitated the increased renal damage. However, even in SHRsp recipients, the native SHRsp kidneys exhibited twice the damage seen in the contralateral transplanted SHR kidneys. CONCLUSION: These data unequivocally demonstrate that the SHRsp kidneys are intrinsically more susceptible than the SHR kidneys to renal damage when exposed to exactly the same BP and metabolic environment.

Animals↗