Table 1.

Phenotypic Analysis

Groups	Body Weight, g	Kidney Weight, g	Urine Protein/Creatinine Ratio	Serum Creatinine, mg%	Adhesions, %	Urine Podocin mRNA/Creat Ratio, units/g Creatinine
TG.1K.ALD (FSGS)	202±7	1.8±0.2	7.3±1.6	1.4±0.1	5.6±2.6	3.1±2.1
TG.2K.ALD	202±15	1.1±0.2a	2.4±0.5a	1.1±0.2	0.0a	0.7±0.3
TG.1K.CRD	144±9a	0.9±0.1a	0.9±0.3a	1.3±0.2	0.0a	1.1±0.2
TG.1K.ALD.Rapa	145±9a	1.1±0.1a	1.1±0.1a	1.7±0.3	0.0a	0.3±0.2b
TG.1K.ALD.ACEi	196±8	1.3±0.1a	1.4±0.2a	1.4±0.2	0.0a	4.4±3.3

Phenotyping for TG rat groups 3 weeks after nephrectomy or sham nephrectomy. Data for the control group before surgery at time 0 is shown at top. The remaining groups were evaluated 3 weeks after surgery (n=5–7 per group). FSGS with adhesions to Bowman’s capsule identified on Masson trichrome–stained sections was observed only in the nephrectomized ad lib–fed group and was associated with greater kidney weight gain and higher level proteinuria. FSGS lesions did not develop if rats did not undergo nephrectomy that caused compensatory kidney hypertrophy, or were prevented from gaining body weight by either calorie reduction or rapamycin treatment, or were treated with ACE inhibitor that did not prevent body weight gain but did prevent kidney enlargement. The rate of podocyte detachment as measured by the urine podocin mRNA/creatinine ratio was not significantly increased by 3 weeks in any group. The statistical comparisons shown compare the four groups that did not develop FSGS to the nephrectomized ad lib–fed group that did develop FSGS. Statistical comparisons by ANOVA with Bonferroni correction. Data are mean±SD. Creat, creatinine; TG, TG rats; 1K/2K, nephrectomized/sham-nephrectomized; ALD, ad lib diet; CRD, 40% calorie reduced diet; rapa, rapamycin-treated; ACEi, treated with angiotensin II inhibitor enalapril.

^aP<0.01.

^bP<0.05.