S1-L1, Renal Physiology (1).pdf

Abdulhassan Alniazy K2,13,18,19 S11,12,15 AB9 L1 OBJECTIVE : 1-FUNCTION OF THE KIDNEY. 2-Endocrine function of kidney. Physiological anatomy of urinary system. The urinary system consists of two kidneys, two ureters, the bladder and a single urethra. The paired kidneys are bean-s...

Abdulhassan Alniazy K2,13,18,19 S11,12,15 AB9 L1 OBJECTIVE : 1-FUNCTION OF THE KIDNEY. 2-Endocrine function of kidney. Physiological anatomy of urinary system. The urinary system consists of two kidneys, two ureters, the bladder and a single urethra. The paired kidneys are bean-shaped retroperitoneal organs, each about 12-cm long and located on the posterior abdominal wall. Each kidney of the adult human weighs about 150 grams and is about the size of a clenched fist. The medial side of each kidney contains an indented region called the hilum through which pass the renal artery and vein, lymphatics, nerve supply, and ureter. Each kidney is surrounded by a tough, fibrous capsule that protects its delicate inner structures. The kidneys extending approximately from the last thoracic vertebrae (T12 ) to third lumbar vertebrae (L3) , receiving some protection from the lower part of the rib cage. The right kidneys is slightly lower than the left one.  Figure1.the urinary system. Supportive tissue of the kidney Three are layers of supportive tissue surround each kidney:  The fibrous capsule, a transparent capsule that prevents infections in surrounding regions from spreading to the kidneys  The perirenal fat capsule, a fatty mass that attaches the kidney to the posterior body wall and cushions it against blows.  The renal fascia, an outer layer of dense fibrous connective tissue that anchors the kidney and the adrenal gland to surrounding structures The fatty encasement of the kidneys is important in holding the kidneys in their normal body position. If the amount of fatty tissue dwindles (as with extreme emaciation or rapid weight loss), one or both kidneys may drop to a lower position, an event called renal ptosis. Renal ptosis may cause a ureter to become kinked, which creates problems because the urine, unable to drain, backs up into the kidney and exerts pressure on its tissue. Backup of urine from ureteral obstruction or other causes is called hydronephrosis. Hydronephrosis can severely damage the kidney, leading to necrosis and renal failure.. Figure 2. Location of the Kidney. Cross section of the abdomen at the level of vertebra L1. Structure of the Kidneys In cross section the kidney had an outer area called the cortex and the inner region the medulla. The medulla is divided into multiple cone- shaped masses of tissue called renal pyramids. The base of pyramid directed to ward the cortex and the tip of pyramid( papilla) projects into the funnel-shaped minor calyces of renal pelvis,. The minor calyces combine to form major calyces, which in turn combine with each other to form the renal pelvis which represent the upper dilated end of the ureter. The walls of the calyces, pelvis, and ureter contain contractile elements that propel the urine toward the bladder.  Figure3: The internal structures of a kidney. Functions of the Kidneys 1. They eliminate the waste products of metabolism, including urea (the main nitrogen-containing end-product of protein metabolism in humans), uric acid (an end-product of purine metabolism), and creatinine (an end-product of muscle metabolism) bilirubin, toxins and other foreign substances. 2. Regulation of water and electrolyte balances; The balance concept state that our body are in balance for any substance when the input and output of that substance are matched. Although we drink water when thirsty, we drink much more because it is a component of beverages that we consume for reasons other than hydration. We also consume food that contains large amounts of water. The kidneys respond by varying the output of water in the urine, thereby maintaining balance for water (ie, constant total body water content). 3. Regulation of arterial pressure; the kidneys play a dominant role in long-term regulation of arterial pressure by excreting variable amounts of sodium and water. The kidneys also contribute to short-term arterial pressure regulation by secreting vasoactive factors or substances, such as renin, that lead to the formation of vasoactive products (e.g., angiotensin II). 4. Regulation of acid-base balance. The kidneys contribute to acid-base regulation, along with the lungs and body fluid buffers, by excreting acids and by regulating the body fluid buffer stores. 5. Regulation of Erythrocyte Production. 6. Regulation of 1,25-Dihydroxyvitamin D3 Production. 7. Gluconeogenesis 8. They degrade several polypeptide hormones, including insulin, glucagon, and parathyroid hormone. ENDOCRINE FUNCTIONS OF THE KIDNEY The kidney is a target organ for several hormones, including antidiuretic hormone (ADH), angiotensin II, aldosterone, atrial natriuretic peptide (ANP), and parathyroid hormone (PTH). The kidney is also an endocrine organ that secretes renin, erythropoietin (EPO), and the active form of vitamin D3, 1,25- dihydroxycholecalciferol (1,25-(OH)2 vitamin D): 1.RENIN SECRETION Renin is an enzyme released by the juxtaglomerular apparatus of the kidney in response to a decrease in effective circulating blood volume. Renin is released from the juxtaglomerular cells lining the afferent arterioles, which respond to reduced renal perfusion, and initiates a cascade of events that result in the production of the hormones angiotensin II and aldosterone. The renin-angiotensin-aldosterone system is the most important endocrine axis in control of the extracellular fluid volume. 2. Erythropoietin (EPO) secretion. EPO is a glycoprotein hormone produced by fibroblasts in the renal interstitium. EPO is released in response to low renal interstitial PO2. It stimulates red blood cell formation in the bone marrow to restore the O2- carrying capacity of blood. About 80% of plasma EPO is produced in the kidney and the remainder is secreted by the liver. The mechanism coupling low PO2 to EPO secretion involves increased local production of prostaglandins. Patients with renal failure do not secrete sufficient amounts of EPO and, therefore, they usually develop anemia. Clinically, the main uses of EPO are related to treating anemia associated with chronic renal failure or to cancer chemotherapy. However, EPO has also gained notoriety in the lay press as a “blood-doping” agent that is used illegally by endurance athletes. In healthy individuals, injection of EPO will lead to supraphysiologic levels of red blood cells (increased hematocrit) and consequently an increase in O2-carrying capacity, a result that boosts aerobic output in athletes during competition. Figure 4: Negative feedback regulation of blood-O2 content via erythropoietin (EPO) secretion. 3.ACTIVATION OF VITAMIN D Vitamin D is a steroid derived from precursors that are either ingested or produced by the action of ultraviolet light on the skin. The active form of vitamin D is 1,25-dihydroxycholecalciferol (1,25-(OH)2 vitamin D). The liver produces 25-hydroxycholecalciferol (25-OH vitamin D), which is converted to 1,25-(OH)2 vitamin D in the kidney under the control of parathyroid hormone. Vitamin D3 promotes Ca2+ conservation in the body by increasing intestinal Ca2+ absorption and also by reducing urinary Ca2+ loss. Figure 5: Renal activation of vitamin D. Manifestations of chronic renal failure plague many of the body’s systems, including bone. Osteitis fi brosa cystica (renal osteodystrophy) is the classic bone disease related to chronic renal failure. The pathophysiologic cascade begins in the kidneys and ends in the bones: 1. As the kidneys fail, so does the function of 1α-hydroxylase, the enzyme that converts inactive 25-OH vitamin D to active 1,25-OH vitamin D, resulting in vitamin D deficiency. 2. Vitamin D deficiency results in low serum Ca2+ due to impaired dietary absorption. 3. Low serum Ca2+ stimulates the parathyroid glands to increase PTH production (secondary hyperparathyroidism). 4. PTH acts on bone to cause a high rate of bone turnover, which releases Ca2+ back into the serum. The end result of this cascade is that near normal plasma Ca2+ concentration is maintained at the expense of chronic bone resorption resulting from hyperparathyroidism. Osteitis fibrosa cystica is a condition characterized by fibrous replacement of the