The Kidney & It’s Collecting System PDF

The Kidney & It’s Collecting System Dr. Erini Serag-Bolos, PharmD Associate Professor USF Taneja College of Pharmacy https://www.vectorstock.com/royalty-free-vector/strong-healthy-kidneys-cartoon-characters-isolated-vector-20632113 Part I Objective...

The Kidney & It’s Collecting System Dr. Erini Serag-Bolos, PharmD Associate Professor USF Taneja College of Pharmacy https://www.vectorstock.com/royalty-free-vector/strong-healthy-kidneys-cartoon-characters-isolated-vector-20632113 Part I Objectives Explain functions of the kidneys Differentiate and discuss the differences between acute renal failure and chronic kidney disease Discuss the differences in etiology and presentation of nephrotic and nephritic syndromes Recognize pathophysiology, presentation, and clinical features of common glomerular diseases Functions of the Kidneys Waste excretion Fluid and electrolyte regulation Maintenance of acid-base homeostasis Secretion of hormones and prostaglandins Calcium homeostasis RBC production  Renal Physiology Renal elimination of drugs and metabolites includes filtration, reabsorption, and active tubular secretion Renal blood flow ~ 1,000 ml/min (60 L/hr) GFR ~ 125 ml/min Urine flow ~1-2 ml/min https://www.youtube.com/ watch?v=oXcEAH_yesY http://moodle.rockyview.ab.ca/mod/book/print.php?id=56711&chapterid=20684  Acute Renal Failure https://fundamentalsofnursingblog.wordpress.com/2016/12/15/acute-kidney-injury/ Chronic Kidney Disease Characterized by progressive deterioration in kidney function with time characterized by irreversible structural damage to existing nephrons Various staging systems to describe extent of disease Protein in the urine as early and sensitive marker for kidney disease End Stage Renal Disease (Stage 5) – requires chronic hemodialysis Leading causes: Uncontrolled diabetes Uncontrolled hypertension Glomerulonephritis Terminology Azotemia – ↑ in blood urea nitrogen (BUN) and serum creatinine (SCr) ↓ glomerular filtration rate (GFR) Pre-renal azotemia – typically due to hypoperfusion of the kidneys Post-renal azotemia – results from obstruction of urine outflow Both are reversible once corrected Uremia – clinical manifestations due to other metabolic and endocrine alterations due to renal damage Systemic biochemical abnormalities caused by azotemia Clinical Manifestations of Renal Diseases – Nephrotic Syndrome Nephrotic syndrome Characterized by: - Proteinuria - Hypoalbuminemia – albumin < 3 g/dL - Edema - Hyperlipidemia Many causes that share common pathophysiology and lead to derangement in capillary walls of the glomeruli ↑ permeability to plasma proteins due to structural or biochemical alterations of the glomerular basement membrane (GBM) Eventually leads to hypoaluminemia  ↓ osmotic pressure  fluid leakage from blood  ↑ extravascular volume  triggers release of renin-angiotensin-aldosterone system (RAAS) to compensate If prolonged proteinuria, salt and water retention aggravates edema and may lead to generalized edema (anasarca) Review of RAAS: https://www.youtube.com/watch?v=PDE2qdS2ZvY Clinical Manifestations of Renal Diseases – Nephritic Syndrome Nephritic Syndrome Characterized by: - Hematuria (due to injured capillary walls by inflammation) - Proteinuria ± edema - Azotemia - Hypertension (due to fluid retention and renin release) Acute onset and caused by inflammation of glomeruli Inflammatory lesions  hematuria  with abundant leukocytes that injure capillary walls  ↓ GFR Functional impairment - GFR reduction manifested by oliguria, fluid retention, and azotemia Caused by: Infection or antibody-mediated: post-streptococcal glomerulonephritis, IgA nephropathy, etc. Systemic disorders (i.e. lupus erythematosus) Clinical Manifestations of Renal Diseases – Nephritic Syndrome Asymptomatic hematuria – IgA nephropathy, Alport syndrome, mild forms of other diseases Rapidly progressive glomerulonephritis (RPGN) – rapid loss of renal function within days or weeks Acute kidney injury (AKI) – abrupt onset of renal dysfunction evidenced by ↑Scr and oliguria/anuria Chronic kidney disease (CKD) – progressive scarring in the kidney characterized by metabolic and electrolyte abnormalities End stage-renal disease (ESRD) – irreversible CKD requiring dialysis or transplantation Urinary tract infection (UTI) – characterized by bacteriuria and leukocytosis Nephrolithiasis – stone formation in the collecting ducts Components of Disease Etiology Discussion of pathophysiology will be divided into four categories due to distinctive manifestation of disease and disease sequelae related to other organ systems Glomeruli Tubules Interstitium Blood vessels  Diseases Affecting the Glomerulus  The Glomerulus Anastomosing network of capillaries in between two layers of epithelium Visceral epithelium (composed of podocytes) – along capillary wall Parietal epithelium – around Bowman’s capsule (urinary space) Bowman’s space (urinary space) – cavity in which filtrate plasma collects https://www.youtube.com/wa tch?v=CMZ2AormwgU https://en.wikipedia.org/wiki/Bowman%27s_capsule The Glomerulus - Components Glomerular capillary – filtration unit Fenestrated endothelial cells Glomerular basement membrane (GBM) – consists of collagen and glycoproteins Lamina densa – thick, electron-dense central layer Lamina rara interna and lamina rara externa – thin, electron-lucent peripheral layers Podocytes – cells with foot process that are embedded in and adherent to lamina rara externa Separated by filtration slits that consist of a protein, nephrin VERY IMPORTANT for selective permeability (diffusion) based on molecular size, charge, and shape Nephrin and podocin maintain selective permeability of the glomerular filtration barrier Mesanglial cells – support the glomerular tuft, capable of proliferation, and secrete mediators in response to cytokines and other factors The Glomerulus - Function Selective permeability to water and small solutes Size: ↑ molecular weight = ↓ permeability Charge: ↑cationic = ↑ permeability Shape Mechanism of Glomerular Injury & Diseases Primary glomerular disease Kidney is the only or predominant organ involved Secondary glomerular disease Injury caused by other systemic diseases  Glomerulonephritis (GN) Caused by Circulating Immune Complexes Immune mechanisms underlie both primary and secondary GN by two possible mechanisms: 1. Deposition of circulating antigen-antibody complexes in the glomerular capillary initiates complement-mediated leukocyte activation Endogenous antigens – systemic lupus erythematosus (SLE) Exogenous antigens – bacterial, viral, parasitic, spirochetal infections The cellular location of the antigen, antibody, or immune complex within the glomerulus determines response to injury Acute injury is short-lived and limited due to degradation or phagocytosis (acute infection- related) Chronic injury due to sustained, repeated cycles of immune complex formation Glomerulonephritis (GN) Caused by Circulating Immune Complexes 2. Immune mechanisms underlie both primary and secondary GN by two possible mechanisms: Antibodies reacting in situ within the glomerulus with intrinsic (fixed) antigens or extrinsic molecules (planted) in glomerulus Planted – from breakdown of apoptotic cells (SLE), bacterial products, or large aggregated proteins (IgG) Anti-Glomerular Basement Membrane Autoantibodies may be directed against protein components of GBM – Goodpasture disease Glomerular Disease by Complement Activation Generates neutrophils and monocytes, leading to GBM degradation and cell damage by oxygen-derived free radicals Arachidonic acid metabolites contribute to GFR reduction Other factors leading to glomerular injury: T lymphocytes, platelets (release prostaglandins), growth factors, nitric oxide, etc. Non-immune Mechanisms of Glomerular Injury Podocyte injury Caused by toxins or poorly characterized circulating factors Results in morphologic changes Clinical outcome: proteinuria Nephron loss Once sufficient nephrons are destroyed to reduce GFR to 30%-50% of normal, symptoms progress to ESRD at varying rates Proteinuria Glomerulosclerosis  Other Diseases Affecting Glomerular Function Disease & Characteristics Pathogenesis Clinical Features Minimal-Change Disease Podocyte injury  proteinuria with -Abrupt development of nephrotic -Relatively benign effacement of foot processes syndrome in otherwise healthy -Most frequent cause of children nephrotic syndrome in Specific process unknown -Favorable prognosis in response pediatrics to corticosteroid therapy; some -Glomeruli maintain normal No antibody deposits become steroid dependent appearance -May occur in adults Focal Segmental -Podocyte injury (unknown cause) -Clinical course and response to Glomerulosclerosis (FSGS) -Primary or secondary etiology therapy very different between -Primary: sclerosis of some (not -May develop after minimal- minimal-change disease and FSGS all) glomeruli; only segments of change disease -Poor response to corticosteroid the glomerulus affected -Associated with nephrotic therapy -Secondary causes: HIV, heroin syndrome, but hematuria and HTN -~50% of patients develop ESRD abuse, secondary to other forms higher in FSGS – mixed picture within 10 years of dx of GN, maladaptation to nephron loss, inherited  Other Diseases Affecting Glomerular Function Disease & Characteristics Pathogenesis Clinical Features Membranous Nephropathy Form of chronic immune complex -Sudden onset -Subepithelial immunoglobulin- glomerulonephritis (GN) due to -Full blown nephrotic syndrome or containing deposits along GBM antibodies reacting to endogenous less degree of proteinuria  thickening of capillary wall or planted glomerular antigens -Does not respond to -Primary disease in ~80 of cases corticosteroid therapy -Secondary causes: infections, Podocyte injury and proteinuria -~40% of patients develop ESRD malignant neoplasms, SLE, within 2-20 years of dx drugs (e.g. captopril, NSAIDs) Membranoproliferative GN Deposition of circulating immune -Presents as nephrotic syndrome (MPGN) complexes or by in situ immune in ~50% of cases -Alterations in GBM and complex formation with a planted -May begin as acute nephritis or mesangium; cell proliferation antigen mild proteinuria -~5-10% of idiopathic nephrotic syndrome cases -MPGN type I > dense deposit dIsease (formerly type II)  Other Diseases Affecting Glomerular Function Disease & Characteristics Pathogenesis Clinical Features C3 Glomerulonephropathy Complement dysregulation due to -Poor prognosis -Two conditions: dense deposit acquired or hereditary -85% recurrence rate in post- disease (formerly MPGN type II) abnormalities of alternative transplantation and C3 glomerulonephritis complement activation pathways -Rare Acute Postinfectious Immune complex disease -Presents as acute nephritic (Poststreptococcal) GN syndrome with edema, HTN, and -Glomerular deposition of Typical case occurs in child 1-4 moderate azotemia immune complexes  weeks after recovery from -Characteristics: hematuria with proliferation and damage to “nephritogenic” of group A smoky brown color glomerular cells and infiltration β-hemolytic streptococcal -Recovery occurs in most of leukocytes infections children; -May also be caused by viral some develop progressive GN diseases (mumps, measles, -15-30% of adults develop ESRD chicken pox, hepatitis B and C) over years to decades  Other Diseases Affecting Glomerular Function Disease & Characteristics Pathogenesis Clinical Features IgA Nephropathy -Attributed to abnormally -Begins as gross hematuria -One of the most common glycosylated IgA1 within 1-2 days of viral URI and causes of GN and recurrent or immunoglobulin, which elicits local pain gross hematuria an autoimmune response -Slow progression to ESRD occurs -Children and young adults -Hereditary predisposition in 25-50% of patients over ~20 -Hallmark sign: deposition of -More common in patients with years IgA in mesangium celiac or liver disease Hereditary Nephritis Mutations within α-chains of type -Alport syndrome: majority of -Group of diseases caused by IV collagen patients have X-linked disease  mutations in genes encoding males affected more frequently GBM proteins and severely than females (likely -Alport syndrome: nephritis + to develop ESRD and deafness) sensorineural deafness and -Female carriers of X-linked Alport eye disorders syndrome or either gender of -Thin basement membrane autosomal forms  typically disease: causes familial asymptomatic and benign clinical hematuria course  Other Diseases Affecting Glomerular Function Disease & Characteristics Pathogenesis Clinical Features Rapidly Progressive -May be caused by multiple -Rapid loss of renal function Glomerulonephritis (RPGN) diseases: -Nephritic syndrome with -Presence of crescents -Anti-GBM antibody-mediated pronounced oliguria and -Immunologically mediated crescentic GN (Goodpasture azotemia -Clinical syndrome disease): clinical pulmonary -If untreated, possible renal failure hemorrhages associated with within weeks to months renal failure; patients benefit from plasmapheresis -Immune complex –mediated crescentic GN -Pauci-immune type crescentic GN References Hudson JQ, Wazny LD. Chronic Kidney Disease. In: Dipiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill. 2017 (available through AccessPharmacy) Kumar V, Abbas A, Aster J. Kidney and It’s Collecting System. In: Robbins Basic Pathophysiology. 10th ed. Philadelphia, PA: Elsevier. 2018 (available through AccessPharmacy) Mason DL, Assimon MM. Chronic Kidney Disease. In: Alldredge BK, Corelli RL, Ernst ME, Guglielmo BJ, Jacobson PA, Kradjan WA, Williams BP. Koda- Kimble and Young’s Applied Therapeutics: The Clinical Use of Drugs. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2013: 764 – 796. Part II The Kidney & It’s Collecting System Dr. Erini Serag-Bolos, PharmD Associate Professor USF Taneja College of Pharmacy https://www.vectorstock.com/royalty-free-vector/strong-healthy-kidneys-cartoon-characters-isolated-vector-20632113 Objectives Recognize the etiology and clinical presentation of acute and chronic pyelonephritis List common medications that may cause tubulointerstitial nephritis (TIN) and characteristics of clinical presentation Recognize pathophysiology, presentation, and clinical features of common renal diseases affecting blood vessels Discuss causes and compensatory mechanisms associated with chronic kidney disease Describe the underlying causes of cystic kidney disease Summarize the presentation and mechanisms of urinary outlet obstruction List common congenital and developmental renal anomalies Recognize the pathophysiology and presentation of common renal malignancies  Diseases Affecting Tubules & Interstitium Diseases Affecting Tubules and Interstitium Tubulointerstitial nephritis (TIN) Glomeruli may be spared or affected later in course of disease Pyelonephritis refers to TIN caused by bacterial infection Interstitial nephritis refers to non-bacterial origin of tubular injury Drugs Metabolic disorders (hyperkalemia, etc.) Radiation Viral infections Immune reactions Acute v. chronic disease designation based on clinical presentation and characteristics  Diseases Affecting Tubules and Interstitium – Acute Pyelonephritis Acute pyelonephritis Inflammation of the kidney and renal pelvis secondary to bacterial infection Manifestation of urinary tract infections (UTIs) Lower UTI – cystitis, prostatitis, urethritis)  most forms of UTI Upper UTI – pyelonephritis Pathogenesis Most commonly enteric G- bacilli E. coli most common causative organism Others: Proteus, Klebsiella, Enterobacter, and Pseudomonas Staph and strep infections less common in acute pyelonephritis  Diseases Affecting Tubules and Interstitium – Acute Pyelonephritis Pathways of renal infection Ascending infection – bacteria reach kidneys from lower urinary tract Most frequent Bacterial adhesion to mucosa  colonization of distal urethra  colonization by and movement against urine flow to reach bladder Urethral instrumentation Hematogenous infection – bacteria reach kidneys through bloodstream Septicemia or infective endocarditis UTI most commonly affects females in absence of instrumentation Colonization due to closely proximity of urethra to rectum or trauma to urethra during sexual intercourse Urine stasis in outflow obstruction or bladder dysfunction may lead to UTI Increased incidence of infection in diabetes, neurogenic bladder dysfunction, and pregnancy Vesicoureteral reflux (VUR) caused by incompetence of vesicoureteral orifice Diseases Affecting Tubules and Interstitium – Acute Pyelonephritis Clinical Features Sudden onset – pain at costovertebral angle S/s of local infection: turbid appearance due to pyuria S/s of systemic infection – chills, fever, nausea, malaise Often unilateral Recurrent or chronic infections may be bilateral Diseases Affecting Tubules and Interstitium – Chronic Pyelonephritis Interstitial inflammation and scarring of renal parenchyma lead to visible scarring and deformity of the pelvicalcyeal system in patients with chronic UTIs Chronic obstructive pyelonephritis Obstruction predisposes kidneys to infection Recurrent infections superimposed on existing obstructive lesions  recurrent renal inflammation and scarring  chronic pyelonephritis May be bilateral (congenital anomalies) or unilateral (renal stones, etc.) Radiological image: affected kidneys are asymmetrically contracted and deformity of calyceal system Chronic reflux-associated pyelonephritis (reflux nephropathy) Most common cause of chronic pyelonephritis Unilateral or bilateral Diseases Affecting Tubules and Interstitium – Drug-Induced Tubulointerstitial Nephritis (TIN) Potential Pathogenesis medications Immune mechanism consistent with hypersensitivity PCNs (ampicillin, reaction methicillin) Latent period between drug exposure and lesion formation – Rifampin eosinophilia and rash Lack of dose dependence for reaction to occur Diuretics Possible recurrence of reaction after re-exposure to the drug or (furosemide) others with similar structure PPIs Cause: IgE (type I) or T cell-mediated (type IV) immune reactions (omeprazole) NSAIDs Clinical features Cimeditine Begins ~15 days after drug exposure Immune Fever, eosiniophilia, rash, renal abnormalities checkpoint Hematuria, leukocyturia inhibitors ↑ SCr or AKI with oliguria Diseases Affecting Tubules and Interstitium – Acute Tubular Injury/Necrosis (ATI) Damage to tubular epithelial cells and acute decline in renal function Shedding of granular casts and tubular cells in urine ↑ SCr and ↓ CrCl Most common cause of AKI and may lead to oliguria (UOP < 400 mL/day) Two forms Ischemic ATI Causes Inadequate blood flow to peripheral organs (hypotension, shock) Secondary to trauma, blood loss, septicemia, pancreatitis, etc. Ischemia to tubules from reduced blood flow (malignant hypertension, microscopic polyangiitis) Hemolytic crises (mismatched blood transfusions, etc.) Nephrotoxic ATI By medications (aminoglycosides), radiographic contrast agents, heavy metals (mercury), organic solvents  Diseases Affecting Tubules and Interstitium – Acute Tubular Injury/Necrosis (ATI) Pathogenesis Proximal tubule epithelial cells sensitive to hypoxemia and vulnerable to toxins Ischemia causes structural alterations in epithelial cells  loss of polarity (reversible)  redistribution of membrane proteins  ↓ sodium reabsorption by proximal tubules  ↑ sodium delivery to distal tubules  afferent vasoconstriction and ↓ in GFR  ↓ perfusion Damaged cells may become detached from basement membranes and shed into urine Build up of tubular debris may block urine outflow  ↑ intratubular pressure  exacerbate GFR decline Fluid from damage tubules may leak back into interstitium  ↓ UOP  ↑ interstitial pressure  tubule collapse Ischemic cells express chemokines, cytokines, and adhesion molecules that recruit leukocytes  interstitial inflammation and tissue injury Necrotic tubular cells elicit inflammatory reaction – further worsens injury and functional derangements Renal vasoconstriction due to endothelial injury  ↓ production of vasodilatory nitric oxide and prostaglandins Diseases Affecting Tubules and Interstitium – Acute Tubular Injury/Necrosis (ATI) Clinical features Patients present with AKI ± oliguria Electrolyte abnormalities Acidosis S/S of uremia and fluid overload Often requires supportive care and hemodialysis Prognosis depends upon underlying disease, comorbidities, etc.  Diseases Affecting Blood Vessels  Diseases Involving Blood Vessels - Nephrosclerosis Sclerosis of small renal arteries and arterioles that is strongly associated with hypertension (HTN) Vascular changes cause ischemia, leading to interstitial fibrosis, tubular atrophy, and focal global glomerulosclerosis Pathogenesis Endothelial dysfunction and platelet activation Thickening of blood vessel wall Extravasation of plasma proteins through injured endothelium and basement membrane deposits Clinical features Functional impairment Mild proteinuria Rarely leads to renal failure except for genetic predisposition among African Americans Diseases Involving Blood Vessels – Malignant Hypertension BP > 200/120 mmHg Pathogenesis – reactions to HTN Injury from long-standing HTN  fibrinoid necrosis and hyperplasia of smooth muscle cells of arterioles Platelet-derived growth factors leads to arteriosclerosis  ↑ BP due to RAAS Clinical features Considered as a medical emergency Papilledema, encephalopathy, cardiovascular abnormalities, renal failure Early symptoms: ↑ intracranial pressure, H/A, N/V, visual impairment All lead to AKI  Diseases Involving Blood Vessels – Thrombotic Microangiopathies (TMAs) Lesions observed in various clinical syndromes characterized by microvascular thrombosis accompanied by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure Endothelial cell injury and platelet activation and aggregation May be caused by toxins, drugs, autoantibodies, or inherited mutations Vessel thromboses within various organs  ischemic injury and organ dysfunction  Diseases Involving Blood Vessels – Thrombotic Microangiopathies (TMAs) Primary forms of TMAs have known etiology (refer to table) Secondary forms caused by: -Malignant HTN -Scleroderma -Pregnancy -Chemotherapy -Anti-phospholipid antibodies -Transplant rejection Diseases Involving Blood Vessels – Thrombotic Microangiopathies (TMAs) Clinical features Shiga toxin-mediated HUS Main cause of AKI in pediatric patients GI/flu-like prodromal symptoms, hematemesis/melena, oliguria, hematuria, hemolytic anemia, possible neurological changes Recovery within weeks with hemodialysis and appropriate treatment Atypical HUS Sudden onset without diarrhea Poorer prognosis than Shiga toxin-mediated HUS Treatment: plasma exchange, liver transplant, antibody inhibitors TTP Sudden onset CNS involvement > kidneys Treatment: plasma exchange to avoid fatality Chronic Kidney Disease (CKD) Final common pathway of progressive nephron loss resulting from any type of kidney disease Scarring and sclerosis of remaining intact nephrons throughout kidneys  ESRD Treatment options include hemodialysis or transplantation Pathogenesis Glomerular hyperfiltration to compensate for reduced GFR due to nephron loss Compensation maintains homeostasis until later stages of CKD Progressive deterioration at variable rate Clinical features Proteinuria, azotemia, HTN Prognosis is poor without treatment, leading to uremia and death Cystic Diseases of the Kidneys Hereditary, developmental, or acquired disorders Underlying defect in the cilia-centrosome complex of tubular epithelial cells Interfere with fluid absorption or cellular maturation Cystic Diseases of the Kidneys Simple cysts – multiple or single lesions of variable size; may have no clinical significance Acquired cystic kidney disease occurs in ESRD after years of dialysis Autosomal dominant (adult) polycystic kidney disease – multiple expanding cysts that affect both kidneys and ultimately destroy the intervening parenchyma Mutation of genes encoding polycystin-1 or polycystin-2 Presentation: fourth decade of life (~10% of ESRD cases), flank pain, intermittent gross hematuria, HTN, UTIs Autosomal recessive (childhood) polycystic kidney disease – rare, autosomal recessive Mutation of gene encoding fibrocystin Presentation: presents at birth; young infants may die or hepatic or renal failure; liver cirrhosis later in life Medullary diseases with cysts Medullary sponge kidney Nephronophthsis-medullary cystic disease complex – most common genetic cause of ESRD in children and young adults Presentation: four variants based on timing of onset; may involve extra-renal manifestations Urinary Outflow Obstruction – Renal Stones (Urolithiasis) Calculus formation anywhere in urinary collecting system; most often in kidney Males > females; hereditary Pathogenesis Calcium oxalate ± calcium phosphate (80%) Increased urinary Magnesium ammonium phosphate (10%) concentration of the Uric acid or cysteine stones (6-9%) stone’s constituents Clinical features No symptoms or renal damage if large stones lodged in renal pelvis Small stones lodged in ureters often painful and associated with gross hematuria Predisposition to bacterial infections due to urine obstruction, ulceration, or bleeding Urinary Outflow Obstruction – Hydronephrosis Dilation of the renal pelvis and calyces with parenchymal atrophy caused by obstruction of urine outflow Causes Congential Acquired: foreign bodies, proliferative lesions, inflammatory lesions, neurogenic, pregnancy Bilateral hydronephrosis occurs if obstruction is below the level of ureters – leads to anuria Congenital and Developmental Anomalies Most common cause of ESRD in patients < 21 years old and accounts for 40-50% of renal failure Typically due to developmental defects of unknown cause Common types Multicystic dysplasia – most common Obstruction in lower urinary tract; gross distortion with variable sizes Renal agenesis Bilateral – incompatible with life Unilateral – uncommon; compatible with normal life in absence of other abnormalities Hypoplasia More commonly unilateral Bilateral results in renal failure in early childhood Has reduced number of renal lobes, but shows no scars  Neoplasms Oncocytoma – benign, arises from collecting ducts; 10% of renal neoplasms Renal cell carcinoma (RCC) – located in the renal cortex 80-85% of primary malignant neoplasms and 2-3% of all adult cancers Types Clear cell carcinomas – 65% of RCCs; have clear cytoplasm Papillary renal cell carcinomas – 10-15% of RCCs; multifocal and bilateral Chromophobe renal carcinomas – 5% of RCCs; from intercalated cells of collecting ducts Typical triad of s/s: painless hematuria, palpable abdominal mass, dull flank pain Common sites of metastasis: lungs and bones Wilms tumor – third most common solid cancer in children; rare in adults Include a variety of cells and tissue components from mesoderm References Hudson JQ, Wazny LD. Chronic Kidney Disease. In: Dipiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill. 2017 (available through AccessPharmacy) Kumar V, Abbas A, Aster J. Kidney and It’s Collecting System. In: Robbins Basic Pathophysiology. 10th ed. Philadelphia, PA: Elsevier. 2018 (available through AccessPharmacy) Mason DL, Assimon MM. Chronic Kidney Disease. In: Alldredge BK, Corelli RL, Ernst ME, Guglielmo BJ, Jacobson PA, Kradjan WA, Williams BP. Koda- Kimble and Young’s Applied Therapeutics: The Clinical Use of Drugs. 10th ed. Philadelphia, PA: Lippincott Williams and Wilkins. 2013: 764 – 796. The Kidney & It’s Collecting System Dr. Erini Serag-Bolos, PharmD Associate Professor USF Taneja College of Pharmacy https://www.vectorstock.com/royalty-free-vector/strong-healthy-kidneys-cartoon-characters-isolated-vector-20632113