Morphological effects of diuretics, of Bartter syndrome, and of NCC knockout on kidney tissue. Note the structural similarities among panels A-C. A: thiazide treatment of rats, from3; focal glomerular injury characterized by wrinkling and thickening of the glomerular basement membrane, with splitting of Bowman's capsule, glomerular collapse, and periglomerular fibrosis (grey arrow). Thickening of peritubular basement membrane in vicinity of the glomerulus (black arrow). Original magnification X630. B: thiazide treatment of rats, from72; dysplasia and degeneration of distal convoluted tubule segments (D) with peritubular inflammation and fibrosis (black arrow), whereas other tubule segments (connecting tubule, CN, and proximal tubule, P) are structurally intact. Magnification X360. C: kidney from Bartter syndrome patient, from74, shows atrophy of one glomerulus (grey arrow) and severe juxtaglomerular hyperplasia affecting a second (black arrow). Magnification X210. D-F: absence of glomerular changes from control (D), metolazone-treated (for 6 days, E), and NCC-knockout mice (F). Panels A, B, and C, used with permission3, 72, 74.