It has long been known that there is a tight relationship between an elevated blood pressure and structural alterations in the kidney. It remains enigmatic, though, whether morphologic renal changes are a primary or a secondary phenomenon. At any rate, in patients with chronic kidney disease (CKD), hypertension by far outweighs other risk factors such as diabetes, obesity, or smoking. Nephropathy in primary hypertension is characterized by fibro-elastic thickening of the intima layer of interlobular arteries and arteriolar hyalinosis. The medial layer may exhibit hyperplasia or remodeling. Low nephron numbers, loss of autoregulation, glomerular hyperfiltration damage, and ultimately glomerulosclerosis due to ischemia and solidification all represent the spectrum of structural changes from the time of being at risk for hypertension to sustained uncontrolled hypertension. Kidney failure is particularly common among patients with malignant hypertension. Here, the renal involvement is likely to be different from that in primary hypertension. Indeed, in these patients, very often secondary causes of hypertension can be found, notably renal parenchymal disease or renal artery stenosis. One of the pathophysiological mechanisms that contribute to the development and maintenance of malignant hypertension is thrombotic microangiopathy. A condition that frequently accompanies CKD is resistance to antihypertensive treatment. Potentially curable causes of treatment resistance in patients with CKD are primary aldosteronism and renal artery stenosis, both of which may have an impact on nephron mass and inflammatory processes within the kidney. The impact of hypertension on the kidney is exemplified by the observation that this abnormality has been identified as the primary cause of kidney replacement therapy in a great deal of patients.