1. Jose L. Rodriguez , MD
Tuesday 6 June 2014
Oshakati Hospital.Namibia.

2.  At the conclusion of this presentation, the
students physician should be able to:
oKnown anatomy of the Kidney
◦ Known about Kidney Function
◦ Describe release three important hormones
◦ Known most common causes of kidney
disease

3.  Nephrology is the study and treatment of kidney disease
. Doctors, nurses and technicians all specialize in
treating patients with kidney disorders. Nephrologists
treat patients with kidney disorders and manage
transplant protocols in hospitals and for transplant
networks. They also manage dialysis centers and
programs. systems to fail.

4. The kidneys are a pair of organs located in the
back of the abdomen. Each kidney is about 4
or 5 inches long -- about the size of a fist.
Each kidney contains around a million units
called nephrons, each of which is a
microscopic filter for blood. It's possible to lose
as much as 90% of kidney function without
experiencing any symptoms or problems.

5.  The kidneys' function are to filter the blood. All the
blood in our bodies passes through the kidneys
several times a day. The kidneys remove wastes,
control the body's fluid balance, and regulate the
balance of electrolytes. As the kidneys filter blood,
they create urine, which collects in the kidneys'
pelvis -- funnel-shaped structures that drain down
tubes called ureters to the bladder.
What do the kidneys do?

7. Am J Kidney Dis 2002; 39:S1

9.  The kidneys are sophisticated reprocessing
machines. Every day, a person’s kidneys process
about 200 quarts of blood to sift out about 2 quarts
of waste products and extra water. The wastes and
extra water become urine, which flows to the
bladder through tubes called ureters. The bladder
stores urine until releasing it through urination.
Am J Kidney Dis 2002; 39(S2): S1-246

10.  People with two healthy
kidneys have 100 percent of
their kidney function. Small or
mild declines in kidney function
—as much as 30 to 40 percent
—would rarely be noticeable.
Kidney function is now
calculated using a blood
sample and a formula to find
the estimated glomerular
filtration rate (eGFR).

11. In addition to removing wastes, the kidneys release
three important hormones:
erythropoietin, or EPO, which stimulates the bone
marrow to make red blood cells
renin, which regulates blood pressure
calcitriol, the active form of vitamin D, which helps
maintain calcium for bones and for normal chemical
balance in the body

12.  Most kidney diseases attack the
nephrons, causing them to lose their
filtering capacity. Damage to the
nephrons can happen quickly, often as
the result of injury or poisoning. But
most kidney diseases destroy the
nephrons slowly and silently. Only after
years or even decades will the damage
become apparent. Most kidney
diseases attack both kidneys
simultaneously.

13.  General
◦ Fatigue & malaise
◦ Edema
 Ophthalmologic
◦ AV nicking
 Cardiac
◦ HTN
◦ Heart failure
◦ Pericarditis
◦ CAD
 GI
◦ Anorexia
◦ Nausea/vomiting
◦ Dysgeusia
 Skin
◦ Pruritis
◦ Pallor
 Neurological
◦ MS changes
◦ Seizures

14. The two most common causes of
kidney disease are diabetes and
high blood pressure. People with a
family history of any kind of kidney
problem are also at risk for kidney
disease.

15.  Diabetes is a disease that keeps
the body from using glucose, a
form of sugar, as it should. If
glucose stays in the blood
instead of breaking down, it can
act like a poison. Damage to the
nephrons from unused glucose
in the blood is called diabetic
kidney disease.

16.  High blood pressure can damage the small
blood vessels in the kidneys. The
damaged vessels cannot filter wastes from
the blood as they are supposed to.
 A doctor may prescribe blood pressure
medication. ACE inhibitors and ARBs have
been found to protect the kidneys even
more than other medicines that lower
blood pressure to similar levels.

20.  GLOMERULAR DISORDERS AND
NEPHROTIC SYNDROMES
 TUBULOINTERSTITIAL DISEASES
 HYPERTENSION
 DIABETES MELLITUS
 URINARY TRACT INFECTION
 OBSTRUTIVE UROPATHY
 CYSTIC KIDNEY DISEASE
 TOXIC DRUGS
 SEVERE INFECTION
 HEREDITARY NEPHROPATHIES

21.  Cockcroft-Gault
◦ Men: CrCl (mL/min) = (140 - age) x wt (kg)
 SCr x 0.81
◦ Women: multiply by 0.85
 MDRD
◦ GFR (mL/min per 1.73 m2
) = 186 x (SCr x 0.0113)-1.154
x
(age)-0.203
x (0.742 if female) x (1.12 if African-American)

22.  Stage 1*: GFR >= 90 mL/min/1.73 m2
◦ Normal or elevated GFR
 Stage 2*: GFR 60-89 (mild)
 Stage 3: GFR 30-59 (moderate)
 Stage 4: GFR 15-29 (severe; pre-HD)
 Stage 5: GFR < 15 (kidney failure)
Am J Kidney Dis 2002; 39 (S2): S1-246

23.  Epoetin alfa (rHuEPO; Epogen/Procrit)
◦ HD: 50-100 U/kg IV/SC 3x/wk
◦ Non-HD: 10,000 U qwk
 Darbepoetin alfa (Aranesp)
◦ HD: 0.45 µg/kg IV/SC qwk
◦ Non-HD: 60 µg SC q2wks

24.  Muscle catabolism
 Metabolic bone disease
 Sodium bicarbonate
◦ Maintain serum bicarbonate > 22 meq/L
◦ 0.5-1.0 meq/kg per day
◦ Watch for sodium loading
 Volume expansion
 HTN

25.  Calcium and phosphate metabolism abnormalities
associated with:
◦ Renal osteodystrophy
◦ Calciphylaxis and vascular calcification
 14 of 16 ESRD/HD pts (20-30 yrs) had
calcification on CT scan
 3 of 60 in the control group
NEJM 2000; 342(20): 1478-83

26.  Abnormalities in the lipid profile
◦ Triglycerides
◦ Total cholesterol
 NCEP recommends reducing lipid levels in high-
risk populations
 Targets for lipid-lowering therapy considered the
same as those for the secondary prevention of CV
disease
JAMA 1993; 269(23): 3015-23

27.  Think about uremia
◦ Catabolic state
◦ Anorexia
◦ Decreased protein intake
 Consider assistance with a renal dietician

28.  70% of HD patients have concomitant CV disease
 Heart disease leading cause of death in HD
patients
 LVH can be a risk factor
Kidney Int 1995; 47(1): 186-92

29.  Patients with CKD (non-HD) have poor
prognosis after MI
 Prospective CCU registry of 1724 pts with
STEMI
 Graded increase in RR of post-infarct
complications: arrhythmia, heart block/asystole,
acute pulmonary congestion, acute MR, and
cardiogenic shock
 Decreased survival over 60 months (RR 8.76;
p<0.0001)
Am J Kidney Dis 2001; 37(6): 1191-200

30.  A week later, you receive the patient’s medical
records…
◦ Ranitidine 150 mg bid
◦ Lisinopril 20 mg daily
◦ Insulin 70/30 25 units SQ bid
◦ EC-ASA 81 mg daily

31.  Four weeks later, the patient returns and
complains of a 1-2 week h/o pedal edema
 His BP today is 159/75 mm Hg
 What now?

32.  BUN/sCr 24/5.4
 Ca+2
7.8
◦ PTH 46.8
 Urine microalbumin (alb/Cr ratio) 5.466
◦ 24 hr urine protein 10,715 mg
 Normal iron studies and SPEP

33.  Maximize control of HTN with ACE/CCB and
hydralazine; use of diuretic for edema
 Maximize control of DM with increasing amounts
of insulin
 Referral to nephrologist for further evaluation:
◦ Six months later, pre-ESRD
◦ On HD in less than one year

34.  Blood
◦ CBC with diff
◦ SMA-7 with Ca2+
and
phosphorous
◦ PTH
◦ HBA1c
◦ LFTs and FLP
◦ Uric acid and Fe2+
studies
 Urine
◦ Urinalysis with
microscopy
◦ Spot urine for
microalbumin
◦ 24-urine collection for
protein and creatinine
 Ultrasound

35.  The serum creatinine level is not enough!
 Target BP for CKD
◦ <130/80 mm Hg
◦ <125/75 mm Hg in proteinuria
 HTN and proteinuria are the two most important
modifiable risk factors for progressive CKD

36. Often what appears to be,
in the end it is not.