2. CHIEF COMPLIANTS
1. Vomiting x 1/12
2. Fever x 1/12
3. Muscle Cramps x 1/12
4. SOB x 1/52
37 year old Male referred to GPHC
from Private Institution two days old
3. History of Presenting Illness
COMPLAINTS DETAILS
VOMITING Gradual Onset, 20 episodes/24hr,
Bitter yellow fluid to meals, no
associated GI Symptoms
FEVER Intermittent, Associated with
Productive Cough, Rx ASA
CRAMPS Hands and Legs would contract, no
fasciculation, paraesthesia
SOB Lying down, ease with sitting,
chest pains on inspiration, 2 pillow
orthopnoea, PND once weekly
4. Past Medical History
Uncontrolled HTN x 7/12
PSHx – nil
Family Hx – DM, HTN
SHx – Alcohol 0, Smoking 0, Driver
Drug Hx – ASA for Fever
Allergies – nil
Blood Transfusions – nil
Trauma - nil
5. Review of Systems
Neuro – Blurred Vision
CVS – Palpitation, Angina on exertion
GU – Frequency, dysuria
MS – Joint Pains
Derm- Itching on Hands and Abdomen
6. Physical Examination
VITAL
S
HR=74, RR= 20, BP= 210/120 , SPO2 =
97% RA
HEENT MM – Pale and Moist
RESP BAE, decreased BS to base, Creps to Base
CVS S1, S2, M0
ABD Globous, depressible, non tender, no
organomegaly, BS+
EXT Nx4, no pretibial oedema
CNS GCS 15/15
7. Impressions
37 year old Male with PMHx of
Uncontrolled Hypertension presents
with symptoms of Uraemia, possible
diagnosis of Chronic Renal Disease
secondary to HTN
9. Background
The term hypertensive nephrosclerosis has
traditionally been used to describe a clinical
syndrome characterized by long-term essential
hypertension, hypertensive retinopathy, left
ventricular hypertrophy, minimal proteinuria, and
progressive renal insufficiency.
In 2009, hypertensive nephrosclerosis (HN)
accounted for 28% of patients reaching end-stage
renal disease (ESRD).
HN is the leading cause of ESRD in Africans (46%)
and the second leading cause of ESRD worldwide.
10. Pathophysiology
Two pathophysiologic mechanisms have been proposed for the
development of hypertensive nephrosclerosis.
(1) Glomerular Ischemia- chronic hypertension results in
narrowing of preglomerular arteries and arterioles, with a
consequent reduction in glomerular blood flow.
(2) glomerular hypertension and glomerular hyperfiltration
- Initial Hypertension leads to glomerular endothelial damage
and sclerosis, subsequently in an attempt to compensate for the
loss of renal function, the remaining nephrons undergo vasodilation
of the preglomerular arterioles and experience an increase in renal
blood flow and glomerular filtration. The result is glomerular
hypertension, glomerular hyperfiltration, and progressive
glomerular sclerosis.
11. Clinical Presentation
HISTORY
In most patients, hypertension is present for many years (usually >10 y),
with evidence of periods of accelerated or poorly controlled BP.
Patients may present with symptoms of Uremia
Nausea
Vomiting
Fatigue
Anorexia
Weight loss
Muscle cramps
Pruritus
Mental status changes
Visual disturbances
Increased thirst
12. Clinical Presentation
PHYSICAL
evidence of hypertension-related target organ damage
includes hypertensive changes in the retinal vessels and
signs of left ventricular hypertrophy.
13. Diagnostic Steps
Blood Tests
CBC, BUN, Cr, Electrolytes, Glucose
Urine Analysis
Microalbuminuria ( 0.5 to 1g / 24hr)
Ultrasound of Kidneys
kidney size is usually symmetric and may be normal or modestly
reduced.
ECG
LVH
RENAL BIOPSY
Diagnsotic, Myointimal hypertrophy of the interlobular arteries,
hyaline degeneration, and sclerosis of afferent arterioles are
the most characteristic findings of hypertensive
nephrosclerosis.
14. Management
Blood Pressure Control
ideal BP of <130/80 mmHg for patients with hypertensive
nephropathy
Several antihypertensive medications, including thiazide diuretics,
beta-blockers, ACE inhibitors, ARBs, and calcium channel blockers,
in principle, can be used as initial monotherapy in patients with
hypertension.
Uremia and CRD
PD or Hemodialysis
Fluid restriction
Epo and iron supplements for anemia
15. Prognosis
The optimal BP goal to slow the progression of renal failure in
patients with hypertensive nephrosclerosis currently is unknown.
Evidence for the beneficial effect of hypertension treatment on
patients with hypertensive nephrosclerosis is lacking, and many
questions regarding the ability of these drugs to protect renal
function in the long term remain unanswered.
hypertensive nephropathy accounts for more than one-third of
patients on hemodialysis and the annual mortality rate for patients
on hemodialysis is 23.3%.
Haemodialysis is recommended for patients who progress to end-
stage kidney disease (ESKD) and hypertensive nephropathy is the
second most common cause of ESKD after diabetes.
