Hypertensive Nephropathy

Hypertensive nephropathy, also known as hypertensive nephroangiosclerosis, is kidney damage caused by chronic arterial hypertension. The interaction between blood pressure and kidney function is complex: hypertension can be both a cause and a consequence of kidney disease, creating a vicious cycle that accelerates organ damage.

Chronic hypertension leads to structural changes in renal vessels from the early stages. Persistent high blood pressure induces thickening of the afferent arterioles, with collagen deposition and fibrosis of the vascular wall. This process, known as nephroangiosclerosis, results in vascular lumen narrowing, reduced glomerular perfusion, and subsequent tissue hypoxia.

Initially, hypertensive nephropathy is asymptomatic, and renal alterations can only be detected through laboratory tests. Microalbuminuria is the first sign of glomerular damage and, if hypertension is not properly managed, progresses to proteinuria, indicating irreversible impairment of the renal filtration barrier.

Hypertensive nephropathy is characterized by a series of histological and functional changes that develop in response to prolonged elevated blood pressure. Structural changes affect renal tissue at the vascular and glomerular levels, while functional consequences manifest as progressive impairment of filtration capacity.

Histological alterations include:

Focal and segmental glomerulosclerosis: some glomeruli undergo sclerosis and obliteration, while the remaining ones undergo compensatory hypertrophy to maintain filtration function.
Arteriolar thickening and interstitial fibrosis: renal arterioles become thickened and less elastic, reducing blood flow and contributing to kidney tissue damage.

The reduction in the number of functioning nephrons leads to renal function deterioration, with progressive impairment of filtration capacity and potential evolution toward chronic kidney disease.

Clinical Manifestations

In its early stages, hypertensive nephropathy is silent and is often diagnosed incidentally during routine check-ups with findings of proteinuria or elevated serum creatinine levels.

As kidney damage progresses, symptoms may include:

Resistant hypertension: kidney impairment contributes to activation of the renin-angiotensin-aldosterone system, further worsening blood pressure levels.
Reduced creatinine clearance: indicative of progressive renal insufficiency.
Peripheral edema and fluid retention: due to glomerular dysfunction and altered sodium balance.
Electrolyte imbalances: particularly hyperkalemia in advanced stages.

In severe cases, hypertensive nephropathy may lead to end-stage renal disease (ESRD), requiring dialysis or kidney transplantation.

Diagnosis

The diagnosis of hypertensive nephropathy relies on various diagnostic tests. Blood tests show elevated serum creatinine and reduced glomerular filtration rate, indicating progressive kidney dysfunction. Urinalysis can detect microalbuminuria in the early stages and proteinuria in advanced cases, signaling significant kidney damage.

Renal ultrasound assesses kidney morphology, revealing reduced renal size and increased vascular resistance, indicative of advanced nephroangiosclerosis. Although rarely indicated, renal biopsy may be performed in cases with uncertain diagnosis or atypical disease progression.

Treatment

Treatment focuses on strict blood pressure control. Maintaining optimal blood pressure levels is the most effective strategy for preventing kidney damage progression and reducing complications.

Additional strategies aim to protect the kidneys and preserve their function.
Proteinuria is a marker of kidney damage and a predictor of disease progression. ACE inhibitors and angiotensin receptor blockers (ARBs), used in hypertension treatment, also have an independent antiproteinuric effect by reducing intraglomerular pressure and counteracting renin-angiotensin system-mediated damage.
For patients with persistent proteinuria, aldosterone antagonists such as Eplerenone and Spironolactone may be added to reduce renal fibrosis and vascular remodeling. Another effective treatment includes SGLT2 inhibitors (Dapagliflozin, Empagliflozin), used for both diabetes and hypertensive nephropathy, as they enhance kidney protection by reducing intraglomerular pressure and proteinuria.
Diet also plays a crucial role. Reducing sodium intake (< 2 g/day) decreases fluid retention and pressure overload. In advanced cases, a low-protein diet helps reduce the metabolic burden on surviving nephrons, slowing disease progression.
When kidney function (GFR) drops below 15% (end-stage), renal replacement therapy becomes necessary. At this stage, options include peritoneal dialysis, allowing blood purification through the peritoneum with home-based procedures, or hemodialysis, an extracorporeal treatment that removes metabolic waste and excess fluids. For eligible patients, kidney transplantation offers a definitive solution, improving long-term quality of life and prognosis.

Conclusion

Hypertensive nephropathy is a leading cause of chronic kidney disease and can progress silently to advanced stages. Early and aggressive blood pressure control is crucial in preventing disease progression. Regular kidney function monitoring in hypertensive patients helps detect nephropathy early and implement targeted therapeutic strategies to preserve renal function.

References

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