Hypertension (HTN) and renal parenchymal disorders are closely interrelated. Available data on HTN in acute renal parenchymal diseases is relatively sparse. Despite changes in vascular reactivity in acute glomerulopathies, abnormal pathological sodium retention has long been identified as the predominant etiology of HTN. The cortical collecting duct appears to be the primary locus, followed by the medullary collecting duct with increased Na+/K+ ATPase activity being the primary mechanism. The target goal BP to be achieved in acute glomerulopathies is not known. Secondary HTN due to obstructive uropathy is reported in both experimental animal models and humans. Sodium retention, increased tubule-glomerular feedback activity, and renin-angiotensin-aldosterone system activation play a predominant role. Prompt decompression of the urinary tract is the most effective way of achieving BP control. There is an abundance of literature in humans suggesting a positive association of renal calculus disease and HTN with significant overlap in the therapeutic management of both disorders. Scleroderma (SSc) is a rare inflammatory connective tissue disorder of the skin and subcutaneous tissues and predominantly occurs in women of childbearing age. Clinical manifestations vary widely depending on internal organs involved. Scleroderma renal crisis (SRC) in essence is a renal thrombotic microangiopathy, ischemic injury being the predominant lesion. The mainstay of therapy is effective and prompt BP control. Angiotensin-converting enzyme inhibitors are the standard of care for all patients with SRC unless there is a definite contraindication such as angioedema. Their use for prevention of SRC has conflicting data and is highly debated.