Jose L. Rodriguez , MDTuesday 6 June 2014Oshakati Hospital.Namibia.

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

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.

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.

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?

Am J Kidney Dis 2002; 39:S1

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

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).

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

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.

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

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.

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.

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.

GLOMERULAR DISORDERS AND NEPHROTIC SYNDROMES

TUBULOINTERSTITIAL DISEASES HYPERTENSION DIABETES MELLITUS URINARY TRACT INFECTION OBSTRUTIVE UROPATHY CYSTIC KIDNEY DISEASE TOXIC DRUGS SEVERE INFECTION HEREDITARY NEPHROPATHIES

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)

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

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 g/kg IV/SC qwk◦ Non-HD: 60 g SC q2wks

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

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

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

Think about uremia◦ Catabolic state◦ Anorexia◦ Decreased protein intake

Consider assistance with a renal dietician

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

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

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

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?

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

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

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

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

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