Urinary & Renal Disorders - Midterm Notes PDF

6 URINARY AND RENAL DISORDERS – Urinary Tract Obstruc/ons Urinary Tract Obstruc/ons Urinary tract obstruc.ons are blockages or restric/ons that impede the flow of urine through the urinary tract. These obstruc.ons can occur at various points along the urinary tract, from the renal pelvis to the uret...

6 URINARY AND RENAL DISORDERS – Urinary Tract Obstruc/ons Urinary Tract Obstruc/ons Urinary tract obstruc.ons are blockages or restric/ons that impede the flow of urine through the urinary tract. These obstruc.ons can occur at various points along the urinary tract, from the renal pelvis to the urethra, and can be classified as upper or lower urinary tract obstruc/on. 1. Most Likely Cause Causes of Upper Urinary Tract Obstruc/on: o Nephrolithiasis (Kidney Stones): Forma.on of crystals, proteins, or other substances (like calcium oxalate, calcium phosphate, uric acid, or struvite stones) within the kidneys or ureters. o Congenital Anomalies: Structural abnormali.es in the urinary tract that obstruct urine flow. o Compression of the Urinary Tract: Can be caused by tumors, pregnancy, or fibrosis surrounding the ureters. Causes of Lower Urinary Tract Obstruc/on: o Prostate Enlargement: Common cause in older males due to benign prosta/c hyperplasia (BPH). o Urethral Stricture: Narrowing of the urethra, oFen due to infec/on, trauma, or scar /ssue. o Pelvic Organ Prolapse: In females, organs such as the bladder, rectum, or uterus may prolapse, leading to bladder obstruc.on. o Bladder Dysfunc/on (Neurogenic Bladder): Neurological condi.ons such as spinal cord injuries can impair the bladder's ability to contract properly. 2. Pathophysiology The pathophysiology of urinary tract obstruc.ons depends on the loca/on, dura/on, and extent of the blockage. 1. Blockage and Pressure Increase: o Obstruc.on of the urinary tract causes urine to accumulate upstream of the blockage. o This increases intraluminal pressure in the affected region, especially in Bowman's capsule, which reduces the glomerular filtra/on rate (GFR), thereby decreasing kidney func.on. o The longer the obstruc.on persists, the greater the likelihood of structural damage, including hydronephrosis (swelling of the kidneys). 2. Hydronephrosis: o Urine backs up into the kidneys, causing dila/on of the renal pelvis and calyces, leading to kidney damage over.me. o Compression of the renal cortex and medulla may lead to renal atrophy and loss of nephrons. 3. Infec/on and Urinary Stasis:  6 1 URINARY AND RENAL DISORDERS – Urinary Incon+nence Urinary Incon+nence (UI) Urinary incon+nence is defined as the involuntary leakage of urine, which can result from a variety of anatomical, neurological, and func+onal disorders. The main types of urinary incon+nence include: 1. Stress Incon+nence 2. Urge Incon+nence 3. Overflow Incon+nence 4. Mixed Incon+nence (combina+on of stress and urge incon+nence) 5. Func+onal Incon+nence (due to physical or cogni+ve impairments). 1. Most Likely Cause The most likely cause of urinary incon+nence depends on the type of incon+nence. The causes for each type are as follows: Stress Incon+nence: o Weakness of the pelvic floor muscles (oFen due to childbirth, pregnancy, aging, or surgery). o Increased intra-abdominal pressure due to ac+vi+es like laughing, coughing, sneezing, or heavy liFing. Urge Incon+nence: o Detrusor overac+vity: Can be triggered by local irrita+on, bladder infec+ons (cys++s), or neurological disorders (e.g., Parkinson's disease, stroke, or spinal cord injury). o Loss of cerebral inhibi+on of detrusor muscle contrac+on. Overflow Incon+nence: o Bladder outlet obstruc+on (due to enlarged prostate, urinary stones, or tumors). o Detrusor underac+vity: Can be caused by spinal cord injury below S1, nerve damage, or medica+ons that impair bladder contrac+on. Func+onal Incon+nence: o Caused by physical or cogni+ve impairments, such as demen+a or limited mobility, which prevent +mely access to a toilet. Mixed Incon+nence: o A combina+on of stress incon+nence and urge incon+nence, oFen seen in older adults. 2. Pathophysiology The pathophysiology of urinary incon+nence varies by type: Stress Incon+nence Pathophysiology: o When intra-abdominal pressure rises suddenly (e.g., from laughing or sneezing), urine leaks because the urethral sphincter is unable to remain closed.  6 1 URINARY AND RENAL DISORDERS – Urinary Tract Infec.ons A urinary tract infec,on (UTI) is an infec+on that affects any part of the urinary system, including the urethra, bladder, ureters, and kidneys. UTIs can be classified into lower UTIs (affec+ng the urethra and bladder) and upper UTIs (affec+ng the kidneys and ureters). 1. Most Likely Cause The most common cause of UTIs depends on the type and loca+on of the infec+on. Causa,ve Microorganism: o Escherichia coli (E. coli) is the most common causa+ve agent for both lower (cys++s) and upper (pyelonephri+s) UTIs. o Other microorganisms include Proteus species, Enterobacter species, and Klebsiella pneumoniae. o In children, especially during the neonatal period, UTIs may also be linked to congenital renal abnormali+es. 2. Pathophysiology The pathophysiology of UTIs varies depending on whether it is a lower UTI (cys,,s) or an upper UTI (pyelonephri,s). Lower UTI (Cys,,s) 1. Bacterial Invasion: o Bacteria, most oGen E. coli, enter the urinary tract via the urethra and aHach to the bladder's epithelial cells. o The bacteria proliferate, triggering an inflammatory response in the bladder wall. 2. Inflamma,on and Mucosal Injury: o The bladder mucosa becomes inflamed, causing redness, edema, and possible forma+on of pus or exudates. o The inflamma+on s+mulates the detrusor muscle, leading to spasms and symptoms such as urgency and frequency of urina,on. 3. Urine Stasis: o Condi+ons like bladder outlet obstruc+on or incomplete bladder emptying can lead to urine stasis, which allows bacteria to mul+ply and colonize. Upper UTI (Pyelonephri,s) 1. Ascending Infec,on: o Infec+on may spread retrogradely from the bladder to the kidneys via the ureters. o It can also result from hematogenous spread (through the bloodstream). 2. Renal Pelvis Inflamma,on: o Inflammatory mediators and white blood cells (WBCs) infiltrate the renal parenchyma. o This leads to renal edema and poten+ally tubular necrosis, impairing kidney func+on.  6 URINARY AND RENAL DISORDERS – Glomerular Disorders Glomerulonephri,s Overview Glomerulonephri-s refers to inflamma,on of the glomerulus within the kidney. It can be acute or chronic and is a significant cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD). 1. Most Likely Cause The causes of glomerulonephri-s can be categorized into primary (affec-ng the glomeruli directly) or secondary (due to systemic diseases) causes. Primary Causes: o Immunological Responses: § Type II hypersensi,vity: An-bodies aCack specific components of the glomerular basement membrane (as seen in Goodpasture syndrome). § Type III hypersensi,vity: Deposi-on of immune complexes (e.g., post- streptococcal glomerulonephri,s) in the glomerulus, triggering inflamma-on. § Type IV hypersensi,vity: T-cell-mediated injury, although less common o Infec,ons: § Post-streptococcal glomerulonephri,s (PSGN) is a common cause following a Streptococcus infec,on of the throat or skin. o Ischemia: Reduc-on in renal blood flow leads to glomerular damage. o Medica,ons & Toxins: Certain drugs and toxins can injure the glomeruli. o Free Radicals: Oxida-ve stress contributes to glomerular damage. o Vascular Disorders: Condi-ons like hypertension can lead to glomerular injury. Secondary Causes: o Diabetes Mellitus: Leads to diabe,c nephropathy, which is the most common cause of chronic glomerulonephri-s【121:0†source】. o Lupus (SLE): Systemic lupus erythematosus (SLE) can cause lupus nephri,s, a form of glomerulonephri-s【121:1†source】. 2. Pathophysiology The pathophysiology of glomerulonephri-s depends on the cause but generally involves an immune-mediated aRack on the glomerulus. 1. Immune Complex Deposi,on: o An,gen-an,body complexes (Type III hypersensi-vity) deposit in the glomerular basement membrane (GBM) following an infec-on, such as post-streptococcal glomerulonephri,s【121:1†source】. o The deposi-on of immune complexes triggers the ac-va-on of complement proteins, which recruit neutrophils and macrophages that release inflammatory cytokines【121:1†source】. 2. Cell-mediated Injury:  6 1 URINARY AND RENAL DISORDERS – Acute Kidney Injury Acute Kidney Injury (AKI) Acute Kidney Injury (AKI) is defined as a sudden decline in kidney func5on, resul7ng in reduced glomerular filtra7on, fluid and electrolyte imbalances, and accumula7on of nitrogenous waste products in the blood. 1. Most Likely Cause The causes of AKI are classified into three major categories: 1. Prerenal Causes (most common) o Hypoperfusion of the kidneys due to condi7ons such as: § Low blood pressure (hypotension) from hemorrhage, shock, or sepsis. § Hypovolemia (severe dehydra7on or blood loss). § Heart failure or reduced cardiac output, causing inadequate blood flow to the kidneys. 2. Intrarenal Causes (damage within the kidney itself) o Direct damage to the kidney structures, including: § Acute tubular necrosis (ATN) caused by ischemia or nephrotoxins (e.g., drugs, toxins). § Glomerulonephri5s (immune-mediated injury to the glomeruli). § Acute inters55al nephri5s (inflamma7on of the kidney's inters77al space, oKen caused by allergic reac7ons to drugs). 3. Postrenal Causes (blockage of urine flow) o Obstruc5on of urinary ouLlow, which increases pressure in the nephrons, causing injury. Examples include: § Kidney stones (nephrolithiasis). § Prostate enlargement (benign prosta7c hyperplasia). § Tumors or ureteral strictures. 2. Pathophysiology The pathophysiology of AKI differs based on the type (prerenal, intrarenal, or postrenal), but generally follows a sequence of events: 1. Prerenal Pathophysiology (renal hypoperfusion) o Decreased renal blood flow reduces glomerular filtra5on rate (GFR), leading to insufficient blood flow to the nephrons. o Hypoxia in the renal 7ssue causes cell injury and ischemia, which may progress to acute tubular necrosis (ATN) if untreated. o GFR can recover quickly if blood flow is restored. 2. Intrarenal Pathophysiology (direct injury to the kidney) o Injury to renal tubules (as in ATN) results from: § Ischemia: Prolonged prerenal failure progresses to ischemic necrosis of the renal tubular cells. § Nephrotoxins (e.g., certain an7bio7cs, NSAIDs) cause damage to the proximal tubular cells, which are responsible for reabsorp7on.  6 1 URINARY AND RENAL DISORDERS – Chronic Kidney Disease Chronic Kidney Disease (CKD) Chronic Kidney Disease (CKD) is defined as a progressive and irreversible loss of kidney func:on. It is characterized by a glomerular filtra:on rate (GFR) of less than 60 mL/min/1.73 m² for three or more months and affects every body system if le> untreated. 1. Most Likely Cause The most common causes of CKD include: Diabetes Mellitus (Diabe:c Nephropathy): Chronic hyperglycemia leads to injury of the glomerular capillaries due to the deposiEon of advanced glyca:on end-products (AGEs), causing inflammaEon, fibrosis, and eventual loss of nephrons. Hypertension (Hypertensive Nephropathy): High blood pressure causes glomerular hypertension, promoEng vascular sclerosis, which damages the nephron's filtering capacity. Glomerulonephri:s: InflammaEon of the glomeruli damages the filtraEon system, which can lead to chronic kidney disease over Eme. Polycys:c Kidney Disease (PKD): A geneEc disorder characterized by the growth of numerous fluid-filled cysts in the kidneys that gradually replace normal kidney Essue. Autoimmune Diseases: CondiEons such as Systemic Lupus Erythematosus (SLE) can lead to glomerular injury, eventually leading to CKD. 2. Pathophysiology The pathophysiology of CKD involves progressive nephron loss and adaptaEons of the surviving nephrons that ulEmately become maladapEve. 1. Loss of Func:onal Nephrons: o Injury to nephrons due to hypertension, diabetes, or immune response causes the loss of funcEonal nephron units. o The remaining nephrons compensate by increasing their filtraEon rate, a process called glomerular hyperfiltra:on. 2. Hyperfiltra:on Injury: o Over Eme, increased glomerular capillary pressure damages the endothelial cells, leading to podocyte detachment and thickening of the glomerular basement membrane (GBM). o This process leads to proteinuria, which contributes to tubulointers::al inflamma:on and fibrosis. 3. Tubulointers::al Inflamma:on: o FiltraEon of excessive proteins and acEvaEon of tubular cells induce the producEon of inflammatory cytokines. o These cytokines promote fibrosis, angiotensin II upregula:on, and increased producEon of reac:ve oxygen species (ROS), which further injure nephron structures. 4. Fibrosis and Scarring:  2 oChronic injury triggers the producEon of myofibroblasts, which deposit extracellular matrix proteins (collagen), leading to scarring. o This process results in the replacement of normal kidney Essue with fibro:c :ssue, reducing kidney funcEon. 5. Reduced Glomerular Filtra:on Rate (GFR): o As fibrosis progresses, GFR declines. o When the GFR drops below 60 mL/min/1.73 m², the clinical diagnosis of CKD is made. o End-stage renal disease (ESRD) occurs when GFR drops to less than 15 mL/min/1.73 m², and dialysis or kidney transplant becomes necessary. 3. Disease Transmission Transmission: o CKD is not a transmissible disease. It results from chronic disease processes (like diabetes, hypertension, and autoimmune disease) or gene:c muta:ons (as seen in polycysEc kidney disease). o There is no transmission from person to person unless there is a gene:c predisposi:on (e.g., in polycysEc kidney disease). 4. Risk Factors Risk factors for CKD can be classified into modifiable and non-modifiable risk factors. Modifiable Risk Factors Diabetes Mellitus: Poor blood glucose control can lead to diabe:c nephropathy, the leading cause of CKD. Hypertension: High blood pressure increases glomerular capillary pressure, leading to vascular sclerosis and nephron damage. Obesity: Increases metabolic demands on the kidneys, promotes insulin resistance, and raises blood pressure. Proteinuria: Increased protein in the urine is both a marker and a contributor to disease progression. Smoking: Induces vascular dysfuncEon and worsens CKD progression. Chronic Use of Nephrotoxic Drugs: Chronic use of NSAIDs (like ibuprofen) can damage renal tubular cells. Non-Modifiable Risk Factors Age: Aging increases suscepEbility to CKD due to glomerular sclerosis and loss of nephron units. Family History: GeneEc predisposiEons such as polycys:c kidney disease (PKD) increase risk. Ethnicity: African Americans, Hispanic Americans, and NaEve Americans have a higher prevalence of CKD. Gender: Males are more suscepEble to CKD progression than females, possibly due to hormonal influences. Summary Table  3 Criteria Chronic Kidney Disease (CKD) Most Likely Diabetes, Hypertension, GlomerulonephriEs, PKD, Autoimmune diseases. Cause 1. Nephron loss → 2. Hyperfiltra:on injury → 3. Tubulointers::al fibrosis Pathophysiology → 4. GFR decline. Not transmissible. CKD results from chronic disease, geneEcs, or toxic Transmission exposure. Modifiable: Diabetes, hypertension, obesity, smoking, NSAID use. Non- Risk Factors Modifiable: Age, family history, geneEcs (PKD), ethnicity, gender. Clinical Manifesta:ons Asymptoma:c Early Stages: CKD may go undetected unEl significant kidney funcEon is lost. Symptoms of CKD: o Uremia (build-up of urea in blood) leads to faEgue, nausea, and confusion. o Electrolyte Imbalances: Hyperkalemia (high potassium), metabolic acidosis, and fluid overload are common. o Anemia: Decreased producEon of erythropoie:n (a hormone produced by the kidneys) leads to reduced red blood cell producEon. o Cardiovascular Disease: PaEents with CKD are at high risk for cardiovascular complicaEons like le_ ventricular hypertrophy (LVH) and heart failure.  2 o Damaged tubular cells form casts that block urine flow, worsening the injury by increasing intratubular pressure. o In glomerulonephri5s, immune complexes deposit in the glomerulus, triggering inflamma7on and injury, leading to proteinuria and hematuria. 3. Postrenal Pathophysiology (urinary tract obstruc7on) o Urinary obstruc5on (from kidney stones, tumors, or prostate enlargement) increases pressure in the nephrons, which opposes the normal pressure gradient required for filtra7on. o Prolonged obstruc7on leads to hydronephrosis (swelling of the kidney due to backed-up urine) and compression of the renal 7ssue, which damages nephron func7on. 3. Disease Transmission Transmission: o Not transmissible. AKI is a non-infec7ous disease. o However, certain infec5ons (e.g., sepsis) may lead to prerenal AKI due to shock and reduced perfusion. 4. Risk Factors The risk factors for AKI depend on the category (prerenal, intrarenal, or postrenal). Risk Factors for Prerenal AKI Age: Older adults have reduced renal reserve. Dehydra5on: Can result from excessive diarrhea, vomi7ng, or inadequate fluid intake. Shock: Hypotension from trauma, hemorrhage, or sep7c shock can decrease renal perfusion. Heart Failure: Reduced cardiac output decreases blood flow to the kidneys. Use of diure5cs: Excessive diuresis may result in dehydra7on and reduced blood volume. Risk Factors for Intrarenal AKI Medica5ons: Use of nephrotoxic drugs (e.g., aminoglycosides, NSAIDs, contrast agents for imaging) increases risk of ATN. Infec5ons: Infec7ons like glomerulonephri5s can cause immune-mediated injury to the kidneys. Autoimmune diseases: Condi7ons like lupus nephri5s may result in immune complexes that deposit in the kidneys. Sepsis: Sepsis-induced ischemia and endotoxins can damage renal tubules. Risk Factors for Postrenal AKI Kidney Stones (Nephrolithiasis): Stones block the ou[low of urine, leading to hydronephrosis and increased intratubular pressure. Prosta5c Hypertrophy (BPH): Enlargement of the prostate can block urine flow in men, especially older men. Urethral Strictures: May develop as a result of trauma, infec5on, or surgery, increasing the risk of postrenal AKI. Tumors: Cancers that invade or compress the urinary tract can lead to postrenal AKI.  3 Summary Table Criteria Acute Kidney Injury (AKI) Most Likely Prerenal (hypoperfusion), intrarenal (tubular injury), postrenal (obstruc7on). Cause Prerenal: Reduced blood flow → reduced GFR. Intrarenal: Tubular injury Pathophysiology (ischemia, nephrotoxins) → casts, obstruc7on, and backpressure. Postrenal: Obstruc7on increases nephron pressure, reducing filtra7on. Transmission Not transmissible. AKI is not an infec7ous disease. Prerenal: Dehydra7on, hemorrhage, shock, heart failure. Intrarenal: Risk Factors Nephrotoxins, glomerulonephri7s, sepsis. Postrenal: Kidney stones, prosta7c hypertrophy, tumors.  o Type IV hypersensi,vity involves T-cell aCack on glomerular cells, leading to damage【121:1†source】. 3. Direct An,body ARack: o In Type II hypersensi,vity, an-bodies directly target glomerular structures, such as in Goodpasture syndrome, leading to inflamma-on and injury【121:1†source 】. 4. Endothelial Injury: o Endothelial cells lining the glomerular capillaries are injured, and the basement membrane becomes more permeable【121:1†source】. o Increased permeability allows proteins (proteinuria) and red blood cells (hematuria) to leak into the urine【121:1†source】. 5. Reduc,on in Glomerular Filtra,on Rate (GFR): o Damage to glomerular capillaries leads to glomerular swelling and capillary obstruc,on, reducing the GFR【121:1†source】. o Increased pressure in Bowman's capsule occurs, leading to decreased filtra-on 【121:1†source】. 6. Chronic Inflamma,on: o Chronic inflamma,on leads to fibrosis and scar ,ssue forma,on, which further impairs kidney func-on, o[en leading to chronic kidney disease (CKD)【 121:0†source】. 3. Disease Transmission Transmission: o Glomerulonephri-s is a non-infec,ous condi,on and is not directly transmissible between individuals【121:1†source】. o However, infec-ons that trigger immune responses, such as Streptococcus pyogenes infec-ons, may indirectly lead to glomerulonephri-s, but the infec-on itself is transmissible (not the kidney disease)【121:1†source】. 4. Risk Factors Risk factors for glomerulonephri-s depend on whether it is acute or chronic. Acute Glomerulonephri,s Risk Factors Recent Streptococcal Infec,on: Throat or skin infec-on with Streptococcus pyogenes (post-streptococcal glomerulonephri-s)【121:1†source】. Other Bacterial, Viral, or Parasi,c Infec,ons: Infec-ons such as Hepa,,s B, C, and malaria can trigger immune-mediated glomerulonephri-s【121:1†source】. Autoimmune Diseases: Condi-ons like Goodpasture syndrome and systemic lupus erythematosus (SLE) increase the risk of glomerulonephri-s【121:1†source】. Medica,ons & Toxins: Certain NSAIDs, an-bio-cs, and toxins increase risk【 121:1†source】. Vascular Disorders: Condi-ons like hypertension and vasculi,s can cause endothelial injury to the glomerulus【121:1†source】. Chronic Glomerulonephri,s Risk Factors  Diabetes Mellitus: Diabe,c nephropathy is a major risk factor for chronic glomerular injury【121:0†source】. Chronic Infec,ons: Prolonged infec-ons with viruses like Hepa,,s B, C can result in immune complex deposi-on and chronic glomerular injury【121:1†source】. Autoimmune Condi,ons: Chronic lupus (SLE) and rheumatoid arthri,s increase the risk of chronic glomerulonephri-s【121:1†source】. Family History: Gene-c predisposi-on to autoimmune diseases can increase risk【 121:1†source】. Summary Table Criteria Glomerulonephri,s Primary: Immunological responses (Type II, III, IV hypersensi-vity), infec-ons Most Likely (post-strep), toxins, medica-ons, ischemia. Secondary: Diabetes, lupus, Cause chronic infec-ons【121:1†source】. Immune complex deposi-on, an-body-mediated aCack, complement Pathophysiology ac-va-on, endothelial damage, capillary obstruc-on, glomerular permeability changes, and fibrosis【121:1†source】. Not transmissible. However, Streptococcus infec,ons that lead to post- Transmission streptococcal glomerulonephri-s are transmissible【121:1†source】. Acute: Recent strep infec-on, autoimmune diseases (Goodpasture, SLE), Risk Factors drugs/toxins, hypertension. Chronic: Diabetes, lupus, hepa--s B/C, chronic infec-ons, family history【121:1†source】. Nephro,c Syndrome Nephro-c syndrome is a kidney disorder characterized by massive protein loss (proteinuria), hypoalbuminemia, edema, and hyperlipidemia/hyperlipiduria. It results from damage to the glomerular filtra,on barrier, which increases permeability to proteins while maintaining the ability to restrict the movement of red blood cells【121:0†source】. 1. Most Likely Cause The causes of nephro-c syndrome can be classified as primary (idiopathic) or secondary. Primary Causes (Idiopathic) 1. Minimal Change Disease (MCD): o Most common in children. o Damage to podocytes leads to loss of the nega-ve charge on the glomerular basement membrane (GBM), allowing albumin to pass into the urine【 121:0†source】. 2. Focal Segmental Glomerulosclerosis (FSGS): o Sclerosis (scarring) of segments of some glomeruli. o O[en idiopathic but can be linked to HIV infec,on, obesity, and heroin use【 121:0†source】. 3. Membranous Nephropathy: o Caused by immune complex deposi-on on the glomerular basement membrane. o Associated with autoimmune diseases (like lupus), cancer, or certain infec,ons 【121:0†source】. Secondary Causes Diabe,c Nephropathy: Damage to glomerular capillaries caused by chronic hyperglycemia. Systemic Lupus Erythematosus (SLE): Autoimmune aCack on the kidneys. Infec,ons: Hepa--s B, Hepa--s C, HIV, and malaria. Medica,ons: Use of nonsteroidal an--inflammatory drugs (NSAIDs) or penicillamine. Amyloidosis: Deposi-on of amyloid proteins in the kidney【121:1†source】. 2. Pathophysiology The pathophysiology of nephro-c syndrome revolves around injury to the glomerular filtra,on membrane. The filtra-on membrane has three key components: 1. Fenestrated endothelium 2. Glomerular basement membrane (GBM) 3. Podocytes with foot processes (form filtra-on slits)【121:0†source】. Steps in Pathophysiology 1. Glomerular Injury: o Damage to any of the three filtra-on layers increases the permeability of the glomerular capillary wall to large proteins (like albumin)【121:0†source】. o Loss of the nega-ve charge on the GBM further increases protein leakage. 2. Massive Proteinuria:  o Massive proteinuria (≥ 3.5 g/day) occurs as proteins escape from the blood into the urine. o Albumin loss results in hypoalbuminemia, leading to decreased onco,c pressure in the blood【121:0†source】. 3. Edema Forma,on: o The decrease in onco-c pressure causes a shi[ of fluid from the vasculature into the inters--al space, resul-ng in generalized edema (anasarca)【121:0†source 】. o Compensatory ac-va-on of the renin-angiotensin-aldosterone system (RAAS) occurs, promo-ng sodium and water reten-on, further exacerba-ng edema【 121:0†source】. 4. Hyperlipidemia and Lipiduria: o Loss of proteins s-mulates hepa-c produc-on of lipoproteins, resul-ng in hyperlipidemia. o Some of these lipids also pass into the urine, causing lipiduria (presence of lipids in the urine)【121:0†source】. 5. Risk of Thrombosis: o Loss of an-coagulant proteins (like an-thrombin III) through the kidneys increases the risk of thrombosis (e.g., renal vein thrombosis)【121:0†source】. 3. Disease Transmission Transmission: o Not transmissible. Nephro-c syndrome is not an infec-ous disease. o Some of its secondary causes, such as HIV, hepa,,s B, and hepa,,s C, are transmissible. However, nephro-c syndrome itself is a non-communicable disease【121:0†source】. 4. Risk Factors Risk factors for nephro-c syndrome can be divided into modifiable and non-modifiable factors. Modifiable Risk Factors Infec,ons: HIV, hepa,,s B, hepa,,s C, and malaria infec-ons are linked to nephro-c syndrome【121:0†source】. Drug Use: o Intravenous drug use (increases risk of HIV and hepa--s C infec-ons). o Use of nephrotoxic drugs such as NSAIDs and an,bio,cs (like penicillamine) increases risk【121:0†source】. Obesity: Linked to focal segmental glomerulosclerosis (FSGS) due to increased glomerular capillary pressure【121:0†source】. Hypertension and Diabetes: Chronic hypertension and diabetes mellitus increase the risk of developing diabe-c nephropathy, which may present as nephro-c syndrome【 121:1†source】. Toxins: Exposure to certain heavy metals (like mercury) can cause nephro-c syndrome【 121:1†source】. Non-Modifiable Risk Factors Age: Minimal change disease (MCD) is the most common cause of nephro-c syndrome in children, while FSGS and membranous nephropathy are more common in adults【 121:1†source】. Gender: Certain types, like membranous nephropathy, are more common in men【 121:0†source】. Gene,cs: Gene-c muta-ons linked to FSGS and congenital nephro-c syndrome (e.g., muta-ons in NPHS1, NPHS2, or ACTN4 genes)【121:0†source】. Autoimmune Diseases: Diseases like systemic lupus erythematosus (SLE) are risk factors for developing nephro-c syndrome【121:0†source】. Summary Table Criteria Nephro,c Syndrome Primary Causes: Minimal change disease (children), FSGS, membranous Most Likely nephropathy. Secondary Causes: Diabetes, SLE, hepa--s B/C, infec-ons, Cause drugs, amyloidosis【121:0†source】. Glomerular filtra,on barrier injury → loss of nega,ve charge → massive Pathophysiology proteinuria → hypoalbuminemia → edema → RAAS ac,va,on → hyperlipidemia and lipiduria【121:0†source】. Not transmissible. However, infec-ons (HIV, hepa--s B/C) that cause Transmission nephro-c syndrome are transmissible【121:0†source】. Modifiable: Infec-ons (HIV, hepa--s B/C), drug use (NSAIDs, an-bio-cs), obesity, hypertension, diabetes, toxins. Non-Modifiable: Age (children for Risk Factors MCD, adults for FSGS), gene-cs, autoimmune diseases (like lupus), and gender【121:0†source】. Nephri,c Syndrome Nephri,c Syndrome is a type of glomerular disease characterized by hematuria (blood in urine), oliguria (reduced urine output), decreased glomerular filtra,on rate (GFR), and hypertension. It is o[en linked to immune-mediated injury of the glomerular capillaries, causing inflamma-on and disrup-on of the filtra-on barrier【121:0†source】. 1. Most Likely Cause The most likely causes of nephri-c syndrome include: Post-Streptococcal Glomerulonephri,s (PSGN): Occurs a[er infec-on with group A beta-hemoly,c Streptococcus. The infec-on may involve the skin (impe-go) or throat (pharyngi-s)【121:0†source】. Systemic Lupus Erythematosus (SLE): Autoimmune disorder where autoan,bodies form immune complexes that deposit in the glomerulus, leading to inflamma-on (Type III hypersensi-vity)【121:0†source】. IgA Nephropathy (Berger's Disease): Immune complexes containing IgA an,bodies are deposited in the glomerular mesangium, causing inflamma-on【121:0†source】. Goodpasture Syndrome: Autoan-bodies bind to type IV collagen in the glomerular basement membrane, leading to complement ac-va-on and glomerular damage【 121:0†source】. Other Causes: o Rapidly Progressive Glomerulonephri,s (RPGN): Can be caused by vasculi,s (e.g., ANCA-associated vasculi,s) or secondary to other condi-ons like SLE【 121:0†source】. o Henoch-Schönlein Purpura (HSP): Immune complex deposi-on (o[en with IgA) in the glomeruli【121:0†source】. 2. Pathophysiology The pathophysiology of nephri-c syndrome involves immune-mediated injury to the glomerular capillary wall, which results in an increase in permeability, glomerular inflamma-on, and reduced GFR. The main mechanisms include: 1. Immune Complex Deposi,on: o An,gen-an,body complexes get deposited in the glomerular capillary walls, par-cularly in cases of post-streptococcal glomerulonephri,s or SLE (Type III hypersensi-vity)【121:0†source】. o These immune complexes ac-vate the complement system, causing the recruitment of inflammatory cells (e.g., neutrophils)【121:0†source】. o The release of proteoly,c enzymes and reac,ve oxygen species (ROS) damages the glomerular endothelium, basement membrane, and podocytes, increasing the permeability of the filtra-on barrier【121:0†source】. 2. Direct An,body Binding: o In Goodpasture syndrome, autoan-bodies bind directly to type IV collagen in the basement membrane (Type II hypersensi-vity)【121:0†source】.  oThis ac-vates complement, promo-ng cell lysis and recruitment of immune cells, which cause further injury to the glomerular capillary【121:0†source】. 3. Damage to the Glomerular Filtra,on Barrier: o The injury to endothelial cells, basement membrane, and podocytes increases the permeability of the glomerular capillary, allowing red blood cells and proteins to pass into the urine【121:0†source】. o The result is hematuria (red blood cell casts) and mild proteinuria (less than seen in nephro-c syndrome)【121:0†source】. 4. Reduc,on in GFR: o Damage to the glomerular filtra-on barrier and capillary lumen increases pressure in the Bowman’s capsule, leading to reduced filtra-on rate【 121:0†source】. o The reduced GFR results in oliguria (low urine output), fluid reten-on, and hypertension【121:0†source】. 3. Disease Transmission Transmission: o Nephri-c syndrome itself is not a transmissible disease. o However, the underlying infec-ons (e.g., streptococcal pharyngi,s or impe,go) that trigger post-streptococcal glomerulonephri-s are contagious and can be transmiCed via respiratory droplets (pharyngi-s) or skin contact (impe-go)【 121:0†source】. o Goodpasture syndrome, SLE, and IgA nephropathy are not transmissible since they result from autoimmune or gene,c predisposi,ons【121:0†source】. 4. Risk Factors Risk factors for nephri-c syndrome vary depending on the specific cause. The following list includes both general and specific risk factors. General Risk Factors Infec,ons: History of recent streptococcal infec,on (skin or throat) increases the risk of post-streptococcal glomerulonephri,s【121:0†source】. Autoimmune Disorders: Systemic Lupus Erythematosus (SLE) is associated with immune complex deposi-on in glomeruli【121:0†source】. Age: Children are more likely to develop post-streptococcal glomerulonephri,s, while IgA nephropathy o[en affects young adults【121:0†source】. Family History: A family history of IgA nephropathy increases the risk of developing the condi-on【121:0†source】. Gene,c Factors: Muta-ons in genes involved in the immune response can predispose individuals to Goodpasture syndrome or IgA nephropathy【121:0†source】. Environmental Factors: Exposure to certain infec,ons (e.g., viral, bacterial), or toxic chemicals may increase risk【121:0†source】. Summary Table Criteria Nephri,c Syndrome Most Likely Post-Streptococcal Glomerulonephri,s, SLE, IgA nephropathy, Goodpasture Cause syndrome, Henoch-Schönlein Purpura【121:0†source】. Immune injury to glomerular filtra,on barrier → Inflamma,on → Loss of Pathophysiology endothelial integrity → RBCs and proteins leak into urine → Hematuria, oliguria, hypertension【121:0†source】. Not transmissible, but infec-ons (e.g., streptococcal pharyngi-s) that trigger Transmission nephri-c syndrome are transmissible via respiratory droplets or skin contact 【121:0†source】. Infec,ons (streptococcal infec-ons), autoimmune diseases (SLE), age (children for PSGN, adults for IgA nephropathy), family history (IgA Risk Factors nephropathy), and gene,c factors (autoimmune disorders)【121:0†source】. Clinical Manifesta,ons Hematuria: Presence of red blood cell casts in the urine, o[en giving it a brown or "cola- colored" appearance【121:0†source】. Oliguria: Reduced urine output due to decreased GFR【121:0†source】. Hypertension: Due to fluid reten-on from reduced kidney filtra-on【121:0†source】. Edema: Swelling of the face or extremi-es may occur in severe cases【121:0†source】. Proteinuria: Although protein is present in the urine, it is typically less severe than in nephro,c syndrome【121:0†source】.  2 3. Systemic Manifesta,ons: o Symptoms include fever, chills, back pain, and flank pain, along with signs of a lower UTI. 3. Disease Transmission Transmission: o Person-to-person transmission does not occur. o Instead, UTIs arise from bacteria that are already present in the gastrointes,nal tract (like E. coli), which colonize the perineal area and ascend into the urinary tract. o In children, anatomical abnormali+es (like vesicoureteral reflux (VUR)) allow urine to flow backward from the bladder to the kidneys, facilita+ng infec+on. o In healthcare seQngs, use of urinary catheters can introduce bacteria directly into the urinary system. 4. Risk Factors Risk factors for UTIs are different for lower UTIs (cys,,s) and upper UTIs (pyelonephri,s). Risk factors can be classified as modifiable or non-modifiable. Lower UTI (Cys,,s) Risk Factors Modifiable Risk Factors: o Poor hygiene: Wiping from back to front can introduce fecal bacteria (like E. coli) into the urethra. o Urinary Catheters: Prolonged use of catheters provides a direct route for bacterial entry. o Sexual Ac,vity: Sexual intercourse increases the risk of UTI, especially in women. o Dehydra,on: Low fluid intake results in concentrated urine, which promotes bacterial growth. o Use of spermicides or diaphragms: These can alter the normal vaginal flora, increasing the risk of UTI. Non-Modifiable Risk Factors: o Female anatomy: Females have a shorter urethra, allowing bacteria to reach the bladder more easily. o Postmenopausal changes: Decreased estrogen causes atrophy of the urogenital mucosa, impairing the natural defense against infec+on. o Congenital abnormali,es: Structural defects of the urinary tract (like vesicoureteral reflux (VUR)) predispose individuals to recurrent UTIs. Upper UTI (Pyelonephri,s) Risk Factors Modifiable Risk Factors: o Urinary stasis: Incomplete bladder emptying increases the risk of retrograde infec+on to the kidneys. o Indwelling catheters: Bacteria can travel through the catheter and infect the urinary tract. Non-Modifiable Risk Factors:  3 o Sex: Females have a higher risk of developing pyelonephri+s than males due to shorter urethras. o Vesicoureteral Reflux (VUR): Abnormal backward flow of urine from the bladder into the ureters and kidneys, common in children. o Pregnancy: Hormonal changes and pressure from the growing uterus slow urine flow, leading to stasis. o Diabetes Mellitus: Impaired immune responses and glycosuria (glucose in urine) promote bacterial growth. Summary Table Criteria Urinary Tract Infec,on (UTI) Most Likely E. coli (most common), other bacteria: Proteus, Klebsiella, Enterobacter. Cause Cys,,s: Bacteria adhere to and invade the bladder epithelium, causing mucosal inflamma,on and detrusor spasms. Pyelonephri,s: Bacteria ascend Pathophysiology from the bladder to the kidneys, triggering an inflammatory response in the renal pelvis. Not person-to-person. Bacteria from the gut or perineal area ascend the Transmission urethra. Catheters and Vesicoureteral Reflux (VUR) facilitate bacterial ascent. Modifiable: Poor hygiene, sexual ac+vity, dehydra+on, use of catheters, Risk Factors certain contracep+ves. Non-Modifiable: Female anatomy, postmenopause, congenital defects (like VUR), pregnancy, diabetes.  2 o Pelvic floor muscle weakness (caused by aging, childbirth, or surgery) results in reduced support for the bladder and urethra, impairing their ability to maintain con+nence. o Impaired sphincter control prevents proper closure of the urethra. Urge Incon+nence Pathophysiology: o Characterized by overac+vity of the detrusor muscle (involuntary bladder contrac+ons) that result in a sudden, strong urge to urinate. o May be triggered by sensory s+mula+on (local irrita+on, infec+on) or neurological dysfunc+on (e.g., Parkinson's disease, stroke). o Loss of cerebral inhibi+on of detrusor contrac+ons leads to involuntary bladder contrac+ons. Overflow Incon+nence Pathophysiology: o Occurs when bladder pressure exceeds urethral pressure due to a chronic overfilled bladder. o Bladder outlet obstruc+on (e.g., from an enlarged prostate) prevents complete bladder emptying, resul+ng in con+nuous, small-volume leakage (dribbling). o The bladder becomes distended, and con+nuous small dribbling occurs because the sphincter is unable to maintain con+nence against the pressure of the large volume of retained urine. Func+onal Incon+nence Pathophysiology: o There is no dysfunc+on of the urinary system, but the individual cannot physically or cogni+vely access a toilet. o This can be due to cogni+ve impairment (e.g., demen+a) or physical limita+ons (e.g., immobility, frailty). Mixed Incon+nence Pathophysiology: o Combina+on of stress and urge incon+nence: The individual may have a weakened pelvic floor (as in stress incon+nence) and detrusor overac+vity (as in urge incon+nence). 3. Disease Transmission Transmission: o Not transmissible. Urinary incon+nence is a non-infec+ous condi+on. o Some infec+ous condi+ons like urinary tract infec+ons (UTIs) or cys++s can lead to transient incon+nence, but they are not considered transmissible causes of incon+nence. 4. Risk Factors The risk factors for urinary incon+nence can be classified as modifiable and non-modifiable factors. Modifiable Risk Factors  3 Obesity: Increases intra-abdominal pressure, which can contribute to stress incon+nence. Smoking: Causes chronic coughing, which increases abdominal pressure, and may also weaken the pelvic floor muscles. High-impact physical ac+vi+es: Repeated ac+vi+es that increase abdominal pressure (like heavy liFing) may cause stress incon+nence. Diet: Excessive intake of caffeine or alcohol can irritate the bladder and worsen urge incon+nence. Medica+ons: Certain drugs (e.g., diure+cs, seda+ves) can affect the bladder's ability to store or release urine. Urinary Tract Infec+ons (UTIs): Can lead to temporary urge incon+nence. Non-Modifiable Risk Factors Age: Older age is linked to a reduc+on in detrusor muscle func+on, reduced bladder capacity, and an increased risk of stress and urge incon+nence. Gender: Women are more prone to stress incon+nence (due to pregnancy, childbirth, and menopause). Childbirth: Vaginal delivery causes stretching and weakening of the pelvic floor muscles, increasing the risk of stress incon+nence. Neurological Disorders: Condi+ons like stroke, mul+ple sclerosis (MS), Parkinson's disease, and spinal cord injuries can impair the brain's ability to control urina+on, leading to urge incon+nence. Spinal Cord Injury: Lesions below S1 or above the sacral area impair reflexes that control bladder filling and voiding, resul+ng in neurogenic bladder and incon+nence. Prostate Enlargement: Enlarged prostate in men can cause overflow incon+nence by blocking the bladder outlet. Summary Table Criteria Urinary Incon+nence Stress Incon+nence: Pelvic floor weakness, increased abdominal pressure. Most Likely Urge Incon+nence: Detrusor overac+vity, neurological changes. Overflow Cause Incon+nence: Bladder outlet obstruc+on, spinal cord injury. Func+onal Incon+nence: Physical or cogni+ve limita+ons. Stress: Weakened pelvic floor & increased abdominal pressure. Urge: Pathophysiology Overac+ve detrusor contrac+ons. Overflow: Overfilled bladder leaks. Func+onal: Physical or cogni+ve inability to access a toilet. Transmission Not transmissible. Urinary incon+nence is a non-infec+ous condi+on. Modifiable: Obesity, smoking, caffeine, alcohol, medica+ons, UTIs. Non- Risk Factors Modifiable: Age, gender (female), pregnancy, childbirth, spinal cord injury, neurological disorders (e.g., stroke).  Urine stasis increases the risk of urinary tract infec/on (UTI) because stagnant o urine is an ideal environment for bacterial growth. 4. Compensatory Changes: o If only one kidney is affected (unilateral obstruc.on), the unaffected kidney undergoes compensatory hypertrophy, increasing its filtra.on rate to maintain renal func.on. o Long-term obstruc.ons may lead to renal fibrosis and irreversible kidney damage. 3. Disease Transmission Transmission: o Not transmissible. Urinary tract obstruc.ons are mechanical or anatomical problems, not infec.ous diseases. o However, infec/ons secondary to obstruc/on (like pyelonephri/s or cys//s) may be caused by bacteria such as E. coli, which can be transmiSed through contaminated water or direct contact. 4. Risk Factors Risk factors for urinary tract obstruc.ons are related to the development of structural abnormali/es, infec/ons, and neurological dysfunc/ons. Risk Factors for Upper Urinary Tract Obstruc/on Nephrolithiasis (Kidney Stones): o Age, Gender, and Race: Men are at higher risk than women for kidney stones, with middle-aged adults being the most affected. o Geographic Loca/on and Climate: Warm climates promote dehydra/on, which increases the risk of stone forma.on. o Dietary Factors: High intake of sodium, oxalate, or animal protein increases stone risk, while adequate hydra.on reduces it. o Medical Condi/ons: Condi.ons such as hyperparathyroidism or metabolic disorders can increase the levels of calcium, uric acid, or oxalate in the urine, promo.ng stone forma.on. Risk Factors for Lower Urinary Tract Obstruc/on Prostate Enlargement: Affects men aged >50 years, par.cularly those with benign prosta/c hyperplasia (BPH). Pelvic Organ Prolapse: Risk is higher in women who have had mul/ple pregnancies or pelvic surgeries. Urethral Stricture: Occurs due to scar /ssue from trauma, infec.on, or surgical procedures on the urinary tract. Neurogenic Bladder: Neurological condi.ons, such as spinal cord injuries, mul/ple sclerosis (MS), or stroke, may impair bladder control and increase the risk of obstruc.on. Summary Table Criteria Urinary Tract Obstruc/ons Upper tract: Kidney stones, congenital anomalies, tumors, fibrosis. Lower Most Likely tract: Prostate enlargement, pelvic organ prolapse, urethral stricture, Cause neurogenic bladder. Obstruc.on increases pressure in urinary tract → hydronephrosis → renal Pathophysiology dysfunc/on. Urinary stasis increases UTI risk. Not transmissible, but infec.ons resul.ng from obstruc.on (e.g., UTI) may Transmission be caused by E. coli. Upper tract: Age, gender, race, dehydra/on, dietary factors, metabolic Risk Factors disorders. Lower tract: BPH, pelvic prolapse, urethral stricture, neurological condi/ons (MS, stroke, spinal cord injury).