Renal Pathology in Hypertensive Nephrosclerosis - An Overview

Introduction:

The condition known as hypertensive nephrosclerosis is typically linked to long-term hypertension. There are more individual elements involved in addition to the blood pressure level. For instance, the risk of end-stage kidney disease (ESKD) caused by hypertension is approximately eight times higher in Black people; this risk may continue even with "adequate" blood pressure treatment. The identification of a link between two independent sequence variants in the apolipoprotein 1 (APOL1) gene on chromosome 22 and kidney disease in African Americans, including focal segmental glomerular sclerosis and hypertension-related ESKD, provides a much more likely pathophysiologic mechanism and suggests that hypertensive nephrosclerosis in Black patients and White patients may be distinct diseases, even though low birth weight and bias in diagnosis based on the patient's race may be involved. In addition, individuals with normal blood pressure may exhibit numerous histologic characteristics of hypertensive nephrosclerosis.

What Is Renal Pathology in Hypertensive Nephrosclerosis?

A clinical condition that includes progressive kidney failure, limited proteinuria, left ventricular hypertrophy, hypertensive retinopathy, and long-term essential hypertension has historically been referred to as hypertensive nephrosclerosis. For the most part, clinical findings are the only basis for diagnosis. In actuality, the majority of the literature on hypertensive nephrosclerosis is predicated on the idea that the condition is typified by progressive kidney failure in a patient with moderate proteinuria, long-standing hypertension, and no evidence pointing to a different diagnosis.

What Are the Clinical Features?

Individuals may exhibit signs of uremia, heart failure, stroke, or hypertension, along with its consequences. Most nephrosclerosis patients have had hypertension for a long time (sometimes more than ten years), with evidence of spikes in or poor control of their blood pressure (BP).

The following characteristics point to the diagnosis of hypertensive nephrosclerosis:

• Black ethnicity.

• Hypertensive alterations in the retina.

• Heart hypertrophy on the left.

• Chronic or extremely severe hypertension.

• Under 0.5 g/d of proteinuria.

• Diagnosed with hypertension before proteinuria occurs.

• Hypertension before renal failure.

• Absence of signs of any other renal illness.

• The results of the biopsy are consistent with the diagnosis.

What Are the Diagnoses?

The following three goals should be included in a patient's evaluation for hypertension:

• Finding extra risk factors for cardiovascular disease.

• Identifying the specific reasons for elevated blood pressure (BP).

• Searching for indications of end-organ damage.

The following investigations are included in the laboratory evaluation:

• Hematocrit.

• The estimated glomerular filtration rate is a measure of creatinine.

• Potassium in serum.

• Calcium in serum.

• Panel lipid.

• Blood sugar.

• Analyzing urine.

• The ratio of urinary albumin to creatinine.

A 24-hour urinary protein excretion greater than one gram per day has been reported in several patients with biopsy-proven hypertensive nephrosclerosis. However, most patients in the large series had urine protein excretion of less than one gram per day. Proteinuria can rise to the nephrotic range when secondary alterations associated with hyperfiltration in focal segmental glomerulosclerosis (FSGS) occur.

Additional Examinations

Left ventricular hypertrophy is often visible on an electrocardiogram (ECG), while the ailment may not be visible on the ECG tracings. ECG sensitivity for left ventricular hypertrophy detection can be as low as 22 percent.

What Is the Treatment?

• Drug Combination Therapy: Two or more antihypertensive medications, such as calcium channel blockers (CCBs), are recommended based on the patient's cardiac and renal functions.

• Medications: Diuretics, β-receptor blockers, α-blockers, and angiotensin II-1 receptor antagonists (ARBs)/ACEIs. If, at the start of the therapy, there wasevidence of a hypertensive crisis, an intravenous infusion of Sodium nitroprusside was given. Within 24 hours of the course starting, the blood pressure dropped to 160 to 170/100 to110 mmHg. Until the blood pressure stabilized, oral antihypertensive therapy was given, and the intravenous antihypertensive medication was progressively stopped.

• Over the past three decades, there has been a drop in cardiovascular and cerebrovascular mortality rates that is closely correlated with improvements in blood pressure (BP) regulation. According to epidemiologic research, long-term cardiovascular risk is increased by even slight kidney function impairments, typically detected by a serum creatinine level higher than 1.4 mg/dL or an estimated glomerular filtration rate (eGFR) lower than 60 mL/min. These results suggest that nephrosclerosis is a component of widespread vascular disease. According to the National Kidney Foundation, a key component of kidney disease patient's therapy should be lowering their risk of cardiovascular disease.

• Treating hypertension effectively maintains kidney function in individuals with parenchymal renal disease, especially in cases of proteinuric kidney disorders such as diabetic nephropathy. Similarly, encouraging data indicate that antihypertensive medication shields renal function in malignant hypertension patients.

• Surprisingly, it is unclear if managing hypertension can stop hypertensive nephrosclerosis-related end-stage renal disease (ESRD). This is unexpected given that over the past 20 years, the proportion of patients aware of their hypertension has risen from 51 percent to 84 percent. Concurrently, the proportion of patients using antihypertensive drugs rose from 36 percent to 73 percent. Studies have revealed that only 25 to 30 percent of people receiving antihypertensive medication have their blood pressure appropriately managed (< 140/90 mm Hg).

• Research on Black hypertensive individuals has not consistently demonstrated that blood pressure reduction slows the advancement of renal damage. The AASK trial set out to investigate if more stringent blood pressure management could impede the advancement of kidney disease in African American patients.

• Blood pressure dropped in the lower blood pressure group from 152/96 mm Hg to 128/78 mm Hg and in the typical blood pressure goal group from 149/95 mm Hg to 141/85 mm Hg. For most of the follow-up period, mean arterial pressure was kept at a mean separation of roughly 10 mm Hg. Throughout the four-year follow-up period, there was no significant difference in the mean GFR decline between the lower and typical blood pressure groups from baseline to the end.

Conclusion:

In animal models, systemic hypertension unmistakably causes or hastens the development of renal disease. Controlling blood pressure (BP) in these models prevents kidney function from deteriorating and lowers proteinuria. Hypertension substantially predicts a quicker drop in the glomerular filtration rate in a range of primary human renal disorders. In the low-BP group and the conventional blood pressure control group, even slight variations in mean arterial pressure substantially slowed the advancement of renal disease.