TABLE 2.

Descriptive parameters

	Control	CyA	Tac	CyA + Alisk	Tac + Alisk
Body weight, g	19.2 ± 0.5	19.6 ± 0.7	19.2 ± 0.5	18.6 ± 0.3	18.4 ± 0.3
CyA, ng/mL	—	42.52 ± 1.2	—	20.43 ± 1.1	—
Tac, ng/mL	—	—	2.14 ± 0.2	—	1.73 ± 0.2
Serum creatinine, μmol/L	19.5 ± 2.6	31.7 ± 3.6*	33.6 ± 5.4*	26 ± 1.3	23.4 ± 1.7
Urinary protein, g/L	0.30 ± 0.10	0.35 ± 0.05	0.25 ± 0.06	0.30 ± 0.0	0.30 ± 0.04
Blood pressure
Systolic, mm Hg	104.6 ± 2.8	109.4 ± 3.7	107.5 ± 3.3	108.1 ± 3.5	102.0 ± 4.1
Dyastolic, mm Hg	84.3 ± 2.6	85.9 ± 4.3	83.5 ± 3.4	85.6 ± 3.2	80.6 ± 2.6
MAP, mm Hg	91.0 ± 2.6	93.7 ± 4.3	89.2 ± 2.5	93.1 ± 3.3	85.0 ± 4.3

The body weight does not differ significantly between the controls and the treated groups. The trough level of the CNIs was set low enough to avoid a severe nephrotoxicity. Based on the serum creatinine there was already after 3 weeks of CNI treatment a significant deterioration of kidney function, which was abolished by cotreatment with direct renin inhibitor Aliskiren. In all groups, the urinary protein excretion was found under or within the range of microalbuminuria. The tail-cuff method did not reveal any significant difference in blood pressure (systolic, diastolic, and MAP) between the controls and treated groups.

^*P ≥ 0.05 vs. control

MAP indicates mean arterial pressure