KIDNEY AND URINARY TRACT DISEASEDR. ALAA HUSSAIN A. AWN KIDNEY TRANSPLANT NEPHROLOGIST AND SPECIALIST OF INTERNAL MEDICINE
HEADLINES - ANATOMY AND PHYSIOLOGY (kidneys and UT) -Ix. Presenting problems in renal and urinary tract disease.
ANATOMY AND PHYSIOLOGY Adult kidneys are 11-14 cm in length, located in the retroperitoneal area on either side of aorta and IVC. The right kidney is usually a few centimeters lower (because the liver lies above it) ,, Each kidney contain approximately one million nephrons, which receive rich blood supply ( 20-25% of cardiac out put)..
FUNCTIONS OF THE KIDNEYS Excretion of nitrogenous waste products and toxins. Body fluid control. Electrolyte balance. Acid – base balance Endocrine function: 1- erythropoietin production 2- activation of vitamin D 3- renin-angiotensin production
large volumes of an ultrafiltrate of plasma (120 ml/min, 170 litres/day) at the glomerulus, and selectively reabsorbing components of this ultrafiltrate at points along the nephron. The rates of filtration and reabsorption are under the control of many hormonal and haemodynamic signals.
The kidney is the main source of erythropoietin, which is produced by interstitial peritubular cells in response to hypoxia. Replacement of erythropoietin reverses the anaemia of chronic renal failure . The kidney is essential for vitamin D metabolism; it hydroxylates 25-hydroxycholecalciferol to the active form, 1,25- dihydroxycholecalciferol. Failure of this process contributes to the hypocalcaemia and bone disease of chronic renal failure .
Renin is secreted from the juxtaglomerular apparatus in response to 1- reduced afferent arteriolar pressure, 2-stimulation of sympathetic nerves, and 3- changes in sodium content of fluid in the distal convoluted tubule at the macula densa. Renin generates angiotensin II , which causes: 1- aldosterone release from the adrenal cortex, 2- constricts the efferent arteriole of the glomerulus and thereby increases glomerular filtration pressure . 3- induces systemic vasoconstriction. By these mechanisms, the kidneys defend circulating blood volume, blood pressure and glomerular filtration during circulatory shock. However, the same mechanisms lead to systemic hypertension in renal ischaemia.
MECHANISMS OF MICTURITION AND URINARY CONTINENCE Continence is dependent on anatomical structures, and on neurological and muscle (sphincter and detrusor) function. Parasympathetic nerves arising from S2-4 stimulate detrusor contraction, resulting in micturition. Sympathetic nerves arising from T10-L2 relay in the pelvic ganglia and produce detrusor relaxation and contraction of the bladder neck (both via α-adrenoceptors).
The distal sphincter mechanism is innervated by somatic motor fibres from sacral segments S2-4 which reach the sphincter either by the pelvic plexus or via the pudendal nerves. Afferent sensory impulses pass to the cerebral cortex, from where reflex-increased sphincter tone and associated suppression of detrusor contraction inhibits micturition until it is appropriate. These factors operate in a coordinated fashion in the micturition cycle, which has a storage (or filling) phase and a voiding (or micturition) phase . At approximately 75% bladder capacity there is a desire to void. Voluntary control is now exerted over the desire to void, which disappears temporarily.
The act of micturition is initiated first by voluntary and then by reflex relaxation of the pelvic floor and distal sphincter mechanism, followed by reflex detrusor contraction. These actions are coordinated by the pontine micturition centre.
INVESTIGATION OF RENAL AND URINARYTRACT DISEASE TESTS OF FUNCTION IMAGING TECHNIQUES OTHER TESTS (Radionuclide studies, renal Bx.)
Renal excretory function can be assessed by measuring serum levels of compounds excreted by the kidney, commonly the products of protein catabolism (urea and creatinine). Blood urea is a poor guide to renal excretory function as it varies with protein intake, liver metabolic capacity and renal perfusion .
Serum creatinine is more reliable as it is produced from muscle at a constant rate and almost completely filtered at the glomerulus. If muscle mass remains constant, changes in creatinine concentration reflect changes in GFR. However, an increase outside the normal range is typically not seen until GFR is reduced by about 50% , and isolated measurements of serum creatinine may give a misleading impression of renal function, particularly if muscle mass is unusually small (or large).
Urine measurements to derive creatinine clearance provide a reasonable approximation of the GFR . More accurate measurement of GFR is now most easily undertaken by ascertaining the clearance of 51Cr-labelled ethylene diamine-tetra acetic acid (EDTA).
The blood filtered through the glomerulus in a rate of 90-120 cc/min.( 170 L / day) We use the creatinine clearance as approximation of glomerular filtration rate. Creatinine clearance= ( 140-age) wt / (s. creatinine )( 72) Creatinine clearance in Female=___________* 0.85 Cr cl =U Cr * v / S Cr * Time ( min)
URINALYSIS Dipsticks may be used to screen for blood and protein semi- quantitatively . Urine microscopy can detect red cells of glomerular origin and red cell casts, indicative of intrinsic renal disease, white blood cells and bacteria seen in urine infections. Crystals (e.g. of calcium oxalate, cysteine or urate) may be seen in renal calculus disease, although calcium oxalate and urate crystals are also sometimes found in normal urine that has been left to stand. Urine pH can provide diagnostic information in the assessment of renal tubular acidosis persistently low specific gravity will be found in diabetes insipidus .
SHOWING ON THE RIGHT GLOMERULAR BLEEDING WITH MANYDYSMORPHIC FORMS INCLUDING ACANTHOCYTES (TEARDROPFORMS), AND ON THE LEFT BLEEDING FROM LOWER IN THE URINARY TRACT
,ON THE LEFT, PHASE CONTRAST IMAGES SHOW HYALINECASTS, A NORMAL FEATURE OF URINE (× 160). ON THE RIGHT,NUMEROUS RED CELLS AND A LARGE RED CELL CAST IN ACUTE GLOMERULAR INFLAMMATION (× 100, NOT PHASE CONTRAST
Timed urine collections can be used;( 24 h) To measure creatinine clearance as a surrogate for GFR can provide a quantitative measure of urinary protein loss. measure the urinary excretion rates of compounds such as calcium, oxalate and urate that can form renal calculi .
Simple measurement of tubular excretory function can be made by comparison of blood and urine ratios of electrolytes to creatinine. Fractional excretion of sodium (= urinary Na/plasma Na × plasma creatinine/urine creatinine). It is reduced in volume depletion when the tubules are avidly conserving sodium, and increased in the tubular damage associated with acute tubular necrosis.
IMAGING TECHNIQUES Plain X-rays ( KUB) may show the renal outlines , opaque calculi and calcification within the renal tract.