2. DEFINATION
• Hypertensive nephrosclerosis: a renal vascular injury
secondary to long-standing arterial hypertension
• Pathophysiology: chronic hypertension → hypertrophy of
medial and intimal layers → narrowing of afferent arterioles
→ ↓ glomerular blood flow → glomerular and tubular
ischemia → arteriolonephrosclerosis and fibrosis (focal
segmental glomerulosclerosis) → end-stage renal disease
3. RISK FACTORS:
• Hypertensive Nephropathy is mostly brought on by chronic, uncontrolled high
blood pressure. It is a crucial cause because those with a family history of
hypertension or kidney illness are more at risk.
• Age is another risk factor because hypertension is more prevalent in older
people.
• Unhealthy lifestyle choices include a high-salt diet, inactivity, smoking, and
drinking alcohol can raise the risk of hypertensive nephropathy.
• Diabetes, inflammatory illnesses such as lupus and vasculitis, and long-term
infections such as hepatitis B and C can all influence the development of
hypertensive nephropathy.
• Hypertensive nephropathy is a progressive disease, meaning the longer
someone has hypertension, the higher their chance of developing chronic
kidney disease and kidney damage.
4. Symptoms
High blood pressure: Hypertension is frequently the initial sign of
hypertensive nephropathy, and it can be challenging to treat in sufferers.
Swelling: One typical sign of hypertensive nephropathy is oedema or swelling
in the hands, feet, and ankles. The body’s fluid retention brings this on due to
damaged kidneys.
Fatigue: Hypertensive nephropathy can cause fatigue and lethargy. This
results from an accumulation of waste products that the kidneys cannot
remove from the body.
Breathlessness: Hypertensive Nephropathy can accumulate fluid in the
lungs, making breathing difficult.
Urinary changes: Hypertensive nephropathy symptoms include variations in
urine colour, frequency, and volume. urine might
5. Nausea and vomiting: Hypertensive nephropathy can result in
nausea and vomiting due to the accumulated waste products in the
body.
Loss of appetite: Hypertensive nephropathy can cause you to feel
less hungry than normal.
Concentration problems: Hypertensive nephropathy can make it
hard to focus and confuse you.
Muscle cramps: These may happen due to electrolyte imbalance in
the body due to kidney impairment. You may suffer muscle cramps,
especially in your legs, while sleeping. These cramps are one of the
symptoms of hypertensive nephropathy
6. Clinical findings
Initially microalbuminuria and microhematuria
↑ BUN, Cr, and uric acid levels, Electrolyte inblanace
and anemia
Nephrosclerosis with proteinuria (usually < 1 g/day)
and progressive renal failure occur with disease
progression.
7. DX:
Diagnostics: renal biopsy shows vascular, glomerular,
and tubulointerstitial changes
Arterial and arteriolar medial hypertrophy, intimal
thickening, and hyalinosis
Global glomerulosclerosis (more common) or focal
segmental glomerulosclerosis
Tubulointerstitial fibrosis
8. Treatment
• Lifestyle modification should be prescribed to all
patients with elevated blood pressure or
hypertension; however, not all patients diagnosed
with hypertension require pharmacologic therapy.
9.
10. • These relative risk reductions correspond to the following absolute benefits:
antihypertensive therapy for four to five years in patients whose blood pressure is 140
to 159 mmHg systolic or 90 to 99 mmHg diastolic prevents a coronary event in 0.7
percent of patients and a cerebrovascular event in 1.3 percent of patients for a total
absolute benefit of approximately 2 percent.
• Who should be treated with pharmacologic therapy?
• Established clinical cardiovascular disease (eg, chronic coronary syndrome [stable
ischemic heart disease], heart failure, carotid disease, previous stroke, or peripheral
arterial disease), Type 2 diabetes mellitus, Chronic kidney disease, Age 65 years or older,
An estimated 10-year risk of atherosclerotic cardiovascular disease of at least 10
percent.
• Patients who continue to have diastolic BP >90 mm Hg after 3−6 months of
nonpharmacologic therapy should be started on an antihypertensive drug. The decrease
in end-organ damage.
11. • Patients who continue to have diastolic BP >90 mm Hg after 3−6
months of nonpharmacologic therapy should be started on an
antihypertensive drug. The decrease in end-organ damage.
• In the absence of a specific indication or contraindication, diuretics
are still recommended as initial treatment (their mortality benefit is
unsurpassed).
• For stage III HTN, BP >160/100, use a 2-drug combination: diuretic
plus ACE
• inhibitors/ARB/CCB or beta blocker.
• If diuretics do not control the BP, add a second medication: ACE
inhibitors/ARB/CCB or beta blocker.
12. AMERICAN GUIDLINES
Reduction of albuminuria has also been considered as a therapeutic target. Analyses of data from RCTs
(Randomixed Controlled Trial) have reported that changes in urinary albumin excretion are predictors of
renal and CV events. However, there are also studies in which treatment that was less effective at reducing
albuminuria was more effective at reducing CV events 75 and vice versa.
whether reducing albuminuria per se is a proxy for CVD prevention remains unresolved. Patients with CKD
should receive lifestyle advice, especially sodium restriction, and drug treatment when their office BP is >
140/ 90 mmg. Achieving recommended BP targets in CKD usually requires combination therapy, which
should be initiated as a combination of a RAS blocker with a CCB or diuretic in these patients. The
combination of two RAS blockers is not recommended.?" Loop diuretics should replace thiazide diuretics
when the estimated GFR is<30 mL/min/1.73 m. The evidence with respect to BP targets in patients with
CKD is complex. In patients with non-diabetic CKD, one meta-analysis showed that the slowest progression
on CKD was obtained with a treated SBP in the range of 110 - 119 mmHg in patients with albumi-nuria > 1
g/day.
In contrast, in patients with a proteinuria <1 g/day, the lowest risk of developing CKD (not CV risk) was
obtained with an SBP of <140 mmHg , Another systematic review failed to demonstrate that a BP target of
<130/80 mmg improved clinical outcomes more than a target of <140/90 mmg in non-diabetic CKD.
13. • Current evidence suggests that in patients with CKD, BP should be lowered to
<140/90 mmHg and towards 130/80 mmHg. Lifestyle advice, especially sodium
restriction, may be especially effective at aiding BP lowering in patients with CKD.
Because BP lowering reduces renal perfusion pressure, it is expected and not
unusual for
• advice, especially sodium restriction, may be especially effective at aiding BP
lowering in patients with CKD. Because BP lowering reduces renal perfusion
pressure, it is expected and not unusual for eGFR to be reduced by 10 - 20% in
patients treated for hypertension.
• Thus, careful monitoring of blood electrolytes and eGFR is essential, but clinicians
should not be alarmed by the anticipated decline in GFR when treatment is initiated.
This decline usually occurs within the first few weeks of treatment and stabilizes
thereafter. If the decline in GFR continues or is more severe, the treatment should
be stopped, and the patient investigated to determine the presence of renovascu-lar
disease.
14. Initial medication
Choice of initial medication should be based on the following:
Patient's initial blood pressure
SBP 130–139 mm Hg or DBP 80–89 mm Hg (stage 1 hypertension): Consider initial
monotherapy.
SBP ≥ 140 mm Hg or DBP ≥ 90 mm Hg AND an average blood pressure > 20/10 mm Hg
above target
Initiate combination therapy.
Commonly used combinations are an ACEI or ARB PLUS either a dihydropyridine CCB OR
a thiazide-type diuretic.
Additional factors to consider
• Major comorbidities
• Major contraindications
• Adverse effects that may be unacceptable to patients
• Patient race: For Black patients (including individuals with diabetes) without CHF or CKD, initial
antihypertensive therapy should include a thiazide-type diuretic or CCB.
21. Patients with CKD or baseline potassium > 5.5 mEq/L and those
who take potassium supplements or potassium-sparing drugs are at
higher risk of hyperkalemia as an adverse effect from
pharmacological treatment for hypertension.
Do not abruptly discontinue beta blockers or alpha-2 agonists. They
must be slowly tapered to avoid triggering rebound hypertension.
Do not use nondihydropyridine CCBs in patients with HFrEF
because of their myocardial depressant effects.
Beta blockers can mask symptoms of hypoglycemia in patients with
diabetes mellitus.
22.
23. Renal replacement therapy
Renal replacement therapy
Nonoperative (hemodialysis or peritoneal dialysis)
Indications include:
Hemodynamic or metabolic complications that are refractory to
medical therapy, e.g.:
Volume overload or hypertension
Metabolic acidosis
Hyperkalemia
– Serositis: e.g., uremic pericarditis
– Other symptoms of uremia: e.g., signs of encephalopathy
– Refractory deterioration in nutritional status
Operative: kidney transplantation
