Renal Disease PDF - Chapter 16 Highlights

(1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED CHAPTER 16 R...

(1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED CHAPTER 16 Renal Disease Kidney disease is a significant global health issue, affecting over 10% of US adults (>20 million people) with chronic kidney disease Major risk factors include diabetes, hypertension, and autoimmune disorders like lupus Early detection is crucial but challenging since patients are typically asymptomatic until advanced stages The kidneys have multiple vital functions: ◦ Blood filtration ◦ Metabolism and excretion ◦ Endocrine functions ◦ Regulation of fluid, acid-base, and electrolyte balance CHECKPOINT 1. What are some important causes of renal disease? 2. What are some consequences of renal failure? NORMAL STRUCTURE & FUNCTION OF THE KIDNEY ANATOMY, HISTOLOGY & CELL BIOLOGY Here's a summary of the kidney's basic anatomy and structure: The kidneys are located in the retroperitoneal area, with each kidney receiving about 20% of cardiac output through its renal artery. They filter blood to remove wastes and regulate electrolytes and blood volume The nephron is the kidney's basic functional unit, with each kidney containing about 1 million nephrons. Each nephron includes: ◦ A glomerulus (capillary tuft) for blood filtration ◦ A renal tubule that reclaims water and salts The glomerulus structure includes: ◦ Afferent and efferent arterioles ◦ Capillaries lined with endothelial cells (podocytes) ◦ Bowman capsule ◦ Mesangium (space between capillaries) The glomerular capillaries have special features: ◦ Fenestrated endothelium with a negative charge that blocks albumin ◦ Epithelial cells called podocytes with foot processes FIGURE 16–1 Vessels and organs of the retroperitoneum FIGURE 16–2 Structures of the kidney. FIGURE 16–3 The vascular supply of the cortical and juxtamedullary nephrons. PHYSIOLOGY Glomerular Filtration & Tubular Resorption https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 1 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Glomerular Filtration & Tubular Resorption Here's a summary of the glomerular filtration and tubular resorption process: Kidneys filter 100-120 mL/min of blood, with 60-70% of Na+ and most K+ and glucose reabsorbed in the proximal tubule Water is reabsorbed passively along Na+ osmotic gradients The loop of Henle receives about 30 mL/min of filtrate and uses a countercurrent multiplier system for urine concentration The collecting ducts receive 5-10 mL/min of filtrate and are controlled by: ◦ Vasopressin (ADH) for water absorption ◦ Aldosterone for Na+ reabsorption and K+/H+ transport The collecting duct is crucial for final regulation of urine volume, water, Na+, acid-base, and K+ balance Renal Regulation of Blood Pressure & Blood Volume The kidney monitors Na+ levels and blood perfusion pressure through the macula densa and juxtaglomerular apparatus Low Na+ or perfusion pressure triggers the renin-angiotensin-aldosterone system (RAAS): ◦ Renin releases angiotensin I, which converts to angiotensin II via ACE ◦ Angiotensin II increases blood pressure through vasoconstriction and aldosterone stimulation Volume depletion also activates: ◦ The RAAS system to retain Na+ and water ◦ Vasopressin release, which increases water reabsorption in collecting ducts This system can be triggered by: ◦ True volume depletion ◦ Edematous states (heart failure, nephrotic syndrome, cirrhosis) ◦ Renovascular disease Renal Regulation of Acid–Base Balance TABLE 16–1 Characteristics of renal tubular acidosis. Here's a summary of how the kidneys regulate acid-base balance: The kidneys work together with the pulmonary system to maintain acid-base homeostasis When pH drops, the process involves: ◦ Quick pulmonary response (seconds to minutes) to exhale CO2 ◦ Slower kidney response (hours to days) to excrete H+ and replenish bicarbonate Acid excretion primarily occurs in the distal collecting duct, where: ◦ H+ is secreted into the tubular lumen ◦ H+ combines with ammonia to form ammonium, which is then excreted Metabolic acidosis can develop through several mechanisms: Excess endogenous acid production exceeding kidney excretion capacity Ingestion of exogenous acids (like methanol or ethylene glycol) Loss of bicarbonate through kidney or GI tract Administration of large amounts of bicarbonate-depleted solutions Renal Regulation of Potassium Balance Here's a summary of renal potassium regulation: Potassium is primarily regulated in the distal collecting duct through aldosterone-mediated Na+ reabsorption https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 2 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Hypokalemia (low potassium) can occur through: K+ shifting from extracellular to intracellular space (e.g., alkalosis, β-agonist therapy) Extrarenal losses (e.g., diarrhea) Renal losses (especially with diuretic use) Hyperkalemia (high potassium) can develop from: Extracellular potassium shifting (e.g., acidosis) Cellular potassium release (e.g., hemolysis) Increased potassium intake Decreased renal excretion (e.g., kidney failure) Renal Regulation of Ca2+ Metabolism The selected text describes the kidney's role in calcium and phosphate regulation: The kidney converts vitamin D3 to its active form (calcitriol), which increases calcium absorption from the gut It responds to parathyroid hormone (PTH), leading to: ◦ Calcium retention ◦ Phosphate excretion in urine Renal Regulation of Erythropoiesis The selected text explains that erythropoietin is a hormone primarily produced by the kidneys. Here are the key points: Erythropoietin stimulates bone marrow to produce and mature red blood cells Production is triggered by blood oxygen levels monitored in the kidney In kidney disease, erythropoietin production becomes impaired, leading to anemia Anemia typically develops when GFR drops to 30-45 mL/min or less, and is almost always present in end-stage renal disease Regulation of Renal Function The kidney uses multiple mechanisms (physical, hormonal, and neural) to control functions. Vasopressin and the countercurrent multiplier system help concentrate urine to maintain fluid balance Tubuloglomerular feedback regulates GFR by monitoring Na+ levels in the distal tubule: ◦ When high Na+ is detected by the macula densa, it triggers vasoconstriction ◦ This reduces GFR and allows better Na+ reabsorption Blood flow regulation is critical: ◦ Cortical flow must maintain adequate GFR while not overwhelming tubule reabsorption ◦ Medullary flow must be balanced to maintain the countercurrent mechanism without causing anoxic damage CHECKPOINT 3. What are the parts of the nephron, and what role does each play in renal function? 4. How is renal function regulated? 5. What are the nonexcretory functions of the kidney? 6. What are the relationships, if any, between each nonex-cretory function named previously and the kidney’s role in fluid, electrolyte, and blood pressure regulation? OVERVIEW OF RENAL DISEASE ALTERATIONS OF KIDNEY STRUCTURE & FUNCTION IN DISEASE https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 3 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM The selected text describes how renal disease can be classified in two main ways: By location of the lesion (glomerulopathy vs. tubulointerstitial disease) By causative factors (immunologic, metabolic, infiltrative, infectious, hemodynamic, toxic) For glomerular diseases specifically, they can be categorized into two types based on presentation: Nephrotic disorders: Show profound proteinuria without cellular inflammation Nephritic disorders: Show variable proteinuria with red and white blood cells in urine Nephrotic disorders are characterized by immune complex deposits near epithelial cells and foot process changes. FIGURE 16–4 The anatomy of a normal glomerular capillary The selected text describes two key points about kidney injury susceptibility: Nephritic disorders involve immune complex deposits in either the subendothelial area, glomerular basement membrane, or mesangium Three regions of the kidney are particularly vulnerable to injury: ◦ The kidney's blood flow regulation system, as GFR depends on renal blood flow ◦ The renal medulla, due to its low-oxygen environment making it prone to ischemic injury ◦ The glomerulus, which is susceptible to immune complex deposition and complement fixation as it filters blood TABLE 16–2 Kidney diseases by site of injury. MANIFESTATIONS OF ALTERED KIDNEY FUNCTION The selected text describes key manifestations of impaired kidney function: Uremia develops due to poor urea excretion, shown by rising BUN and creatinine levels, leading to various symptoms and lab abnormalities Without proper kidney function, excess intake of electrolytes, water, or acids can cause dangerous imbalances In renal insufficiency, excess sodium intake can lead to volume expansion, resulting in hypertension and heart failure TABLE 16-3 Clinical abnormalities in uremia. CHECKPOINT 7. What characteristics of various parts of the nephron make it particularly susceptible to certain types of injury? 8. What is uremia, and what are its most prominent symp-toms and signs? PATHOPHYSIOLOGY OF SELECTED RENAL DISEASES ACUTE KIDNEY INJURY Clinical Presentation acute kidney injury (AKI) is characterized by: Rapid deterioration of renal function occurring within days to a week, leading to accumulation of nitrogenous wastes in blood Often presents with diminished urine output (oliguria), though this isn't always present Defined by either: ◦ A rise in serum creatinine ≥0.3 mg/dL within 48 hours, or ◦ Urine output falling below 0.5 mL/kg/h for 6+ hours TABLE 16–4 Initial clinical and laboratory data base for defining major syndromes in nephrology. Etiology https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 4 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM A. Prerenal Causes The selected text explains the Starling equation and glomerular filtration process: Glomerular filtration is determined by both hydrostatic and oncotic pressures in the glomerular capillary and tubular lumen Key factors include: ◦ Glomerular permeability (Kf) ◦ Osmotic pressure contribution (σ) ◦ Intracapillary and intratubular pressures (both hydrostatic and oncotic) A unique feature of the kidney is its ability to autoregulate blood flow through both afferent and efferent arterioles, unlike other capillary beds which can only regulate incoming flow. Changes in renal blood flow or afferent artery constriction can affect intracapillary hydrostatic pressure and thus filtration B. Intrarenal Causes The selected text describes the intrarenal causes of acute kidney injury (AKI), which can be divided into two main categories: Inflammatory diseases - including vasculitis, glomerulonephritis, and drug-induced injury Acute tubular necrosis - caused by ischemia and toxic injury Key points about intrarenal AKI: Common toxic causes include aminoglycoside antibiotics and rhabdomyolysis (where muscle protein myoglobin damages tubules) Sepsis is a major cause, involving both prerenal factors (hypoperfusion) and intrarenal damage from cytokine dysregulation Sepsis patients are at additional risk due to exposure to nephrotoxic drugs and contrast agents used in imaging C. Postrenal Causes The selected text describes postrenal causes of acute kidney injury (AKI), which occur due to urinary tract obstruction. There are two main types: Intrinsic obstruction - such as kidney stones blocking the ureter Extrinsic obstruction - such as when an external mass compresses the ureter TABLE 16–5 Major causes of acute kidney injury. Pathology & Pathogenesis The text describes two main theories for acute kidney injury: Tubular Theory: Cellular debris forms casts that block tubular lumens, increasing pressure and reducing filtration Vascular Theory: Changes in arteriolar blood flow reduce glomerular perfusion pressure and filtration Key effects of hypoxia include: Disordered cell adhesion leading to tubular obstruction Disruption of cellular connections causing filtrate leakage and channel dysfunction Increased damage due to medullary hypoxia and inflammatory factors (cytokines, endothelins) FIGURE 16–5 Pathophysiology of ischemia-induced acute kidney injury. Clinical Manifestations Early kidney injury symptoms include fatigue and malaise due to impaired excretion of water, salt, and wastes. As the condition progresses, patients develop breathing difficulties, abnormal heart sounds, and swelling. Early treatment can improve kidney blood flow and prevent acute tubular necrosis. Without intervention, the condition may worsen and require dialysis during the extended recovery period. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 5 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM CHECKPOINT 9. What are the features that distinguish prerenal, intrare-nal, and postrenal causes of renal failure? 10. What are the current theories for the development of acute tubular necrosis? 11. What clues are helpful in determining whether newly diagnosed renal failure is acute or chronic? 12. What is the natural history of acute kidney injury? TABLE 16–6 Causes of acute kidney injury in which FENa+ may be below 1% CHRONIC KIDNEY DISEASE Clinical Presentation The selected text explains that chronic kidney disease (CKD) patients experience a wide range of symptoms and laboratory abnormalities that go beyond what's seen in acute kidney injury. These extensive symptoms occur because CKD is a long-term, progressive condition that affects multiple body systems. Key facts about CKD from the surrounding context: The most common cause is diabetes mellitus, followed by hypertension The disease involves: ◦ Loss of kidney function that can progress to uremia ◦ Significant functional reserve - up to 50% of nephrons can be lost before showing impairment ◦ High risk of complications when stressed by infection, dehydration, or nephrotoxic drugs Etiology Diabetes is the leading cause of CKD, with hypertension being the second most common cause, while glomerulonephritis (GN) ranks third. TABLE 16–7 Prevalence by etiology for U.S. Medicare–treated end-stage renal disease for 2014. Pathology & Pathogenesis Development of Chronic Kidney Disease The selected text explains the key differences between acute and chronic kidney injury: While acute kidney injury involves temporary damage where cells can regenerate, chronic kidney injury leads to permanent nephron loss This loss creates a cycle where: ◦ Remaining nephrons face increased filtration pressure ◦ This leads to glomerular sclerosis (scarring) ◦ Results in accelerated nephron destruction and progression to uremia Important notes: The kidneys have significant reserve capacity - up to 50% of nephrons can be lost before showing functional impairment However, patients with reduced function are vulnerable to uremia when faced with additional stressors like infection, dehydration, or nephrotoxic drugs https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 6 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Pathogenesis of Uremia The pathogenesis of uremia involves three main factors: 1. Accumulation of substances normally excreted by kidneys (like nitrogen-containing products) 2. Increased levels of normal hormones 3. Loss of normal kidney products (like erythropoietin) Additionally, uremia causes fluid and electrolyte imbalances, resulting in increased intracellular sodium and water, while decreasing intracellular potassium. Clinical Manifestations A. Na+ Balance and Volume Status The selected text describes sodium and fluid balance in Chronic Kidney Disease (CKD): CKD patients typically retain excess sodium and water due to impaired kidney excretion Excessive sodium intake can lead to complications like: ◦ Heart failure ◦ Hypertension ◦ Peripheral edema ◦ Weight gain Recommended management includes: ◦ Limiting sodium intake to 2g/day or less ◦ Restricting fluid intake to urine output plus 500mL B. K+ Balance The selected text describes hyperkalemia (high potassium) in Chronic Kidney Disease (CKD): It's a potentially life-threatening complication, especially in advanced CKD with GFR below 15 mL/min Early in CKD, the body compensates through increased aldosterone-mediated potassium transport However, certain medications can trigger dangerous hyperkalemia in CKD patients, including: ◦ K+-sparing diuretics ◦ ACE inhibitors ◦ β-blockers C. Metabolic Acidosis This passage describes metabolic acidosis in Chronic Kidney Disease (CKD): Caused by reduced ability to excrete acid and generate base in CKD For patients with GFR above 20 mL/min: ◦ Only moderate acidosis typically develops ◦ Can be treated with 20-30 mmol of oral sodium bicarbonate daily These patients are at high risk for acidosis during: ◦ Sudden acid load (ketoacidosis, lactic acidosis, toxic ingestions) ◦ Bicarbonate loss (like diarrhea) D. Mineral and Bone The passage describes bone disorders in Chronic Kidney Disease (CKD), which develop through five key mechanisms: 1. Reduced calcium absorption from the gut https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 7 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM 2. Excessive PTH production 3. Disrupted vitamin D metabolism 4. Phosphorus retention 5. Chronic metabolic acidosis These factors collectively lead to increased bone resorption. FIGURE 16–6 Pathogenesis of bone diseases in chronic kidney disease. E. Cardiovascular and Pulmonary Abnormalities The selected text describes key cardiovascular complications in Chronic Kidney Disease (CKD): Heart failure and pulmonary edema can occur due to volume and salt overload Hypertension is common and has two main causes: ◦ Fluid and sodium overload ◦ Hyperreninemia (overproduction of renin by failing kidneys) Cardiovascular disease is the leading cause of death in CKD patients F. Hematologic Abnormalities The selected text describes two major hematologic complications in Chronic Kidney Disease (CKD): Anemia: Characterized by normochromic and normocytic features, primarily caused by decreased erythropoietin production leading to reduced red blood cell formation Bleeding abnormalities: Patients experience: ◦ Increased bruising and decreased clotting ◦ Higher risk of spontaneous GI and cerebrovascular hemorrhage ◦ Multiple laboratory abnormalities including prolonged bleeding time and abnormal platelet function ◦ These issues persist even with dialysis treatment CHECKPOINT 13. What is the mechanism by which altered sodium, potas-sium, and volume status develop in chronic kidney disease? 14. What are the most common causes of chronic kidney disease? GLOMERULONEPHRITIS & NEPHROTIC SYNDROME Clinical Presentation & Etiology Glomerulonephritis (GN): Disorders resulting in glomerular disease typically fall into one of several categories of clinical presentation. However, there can be overlap among these categories: 1. Acute GN Characterized by: ◦ Sudden onset of hematuria (blood in urine) and proteinuria (protein in urine) ◦ Reduced glomerular filtration rate (GFR) ◦ Retention of salt and water ◦ Common trigger: infections, particularly strep infections of the throat or skin (from "nephritogenic" strains of group A β- hemolytic streptococci) TABLE 16–8 Causes of acute glomerulonephritis. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 8 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM 2. Chronic glomerulonephritis Characterized by: Persistent urinary abnormalities Slow progressive decline in renal function over years Does not typically resolve Can lead to end-stage renal disease within 20 years of discovering abnormal urinary sediment 3. Nephrotic syndrome Characterized by: Marked proteinuria (especially albuminuria with 24-hour urine protein excretion >3.5g) Hypoalbuminemia https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 9 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Hypoalbuminemia Hyperlipidemia Edema The underlying causes of nephrotic syndrome are often not clear. 4. Asymptomatic urinary abnormalities Is characterized by: Presence of hematuria and proteinuria (at levels lower than nephrotic syndrome) No functional abnormalities in terms of: Reduced GFR Edema Hypertension This is one of the four main categories of glomerular disease presentation. TABLE 16–9 Glomerular causes of asymptomatic urinary abnormalities. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 10 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Pathology & Pathogenesis The underlying causes of glomerulonephritis (GN) and nephrotic syndrome: These conditions are believed to result from immune- mediated renal damage, with variations in their presentation depending on the specific nature and extent of the damage. Both genetic factors and environmental triggers play a role in activating the immune response, though these environmental triggers are not well understood. TABLE 16–10 Location of electron-dense deposits in glomerular disease. A. Acute and Rapidly Progressive Glomerulonephritis The selected text describes how acute glomerulonephritis (GN) is classified and diagnosed using multiple diagnostic techniques: Light microscopy is used to identify areas of injury Classification into subgroups is done using a combination of: Circulating autoantibodies Complement deposition measurements Immunofluorescence studies https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 11 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Immunofluorescence studies Electron microscopy B. Chronic Glomerulonephritis The selected text describes how chronic glomerulonephritis (GN) can develop from acute GN over 5-20 years, with three main pathological patterns: Cellular proliferation in the mesangium or capillary Sclerosing chronic GN - characterized by obliteration of glomeruli Membranous GN - showing irregular subepithelial proteinaceous deposits affecting glomeruli uniformly C. Nephrotic Syndrome The text describes key features of nephrotic syndrome pathology: The podocyte is the primary target of injury Light microscopy shows minimal changes to the glomerulus, with little to no inflammation Immunofluorescence testing reveals antigen-antibody complex deposits in the glomerular basement membrane TABLE 16–11 Clinical and histologic features of idiopathic nephrotic syndrome. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 12 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Clinical Manifestations In glomerulonephritic diseases: ◦ Damage to glomerular capillary walls causes leakage of red blood cells and proteins, leading to hematuria and proteinuria ◦ Decreased GFR occurs due to inflammatory cell infiltration or restricted blood flow ◦ Results in fluid/salt retention, causing edema and hypertension In nephrotic syndrome: ◦ Patients experience hypoalbuminemia and decreased plasma oncotic pressure due to protein loss in urine ◦ Despite showing signs of volume overload (edema), patients can develop intravascular volume depletion leading to syncope, shock, and acute kidney injury CHECKPOINT 15. What are the categories of glomerulonephritis, and what are their common and distinctive features? 16. What are the pathophysiologic consequences of nephrotic syndrome? RENAL STONES Clinical Presentation Renal stones typically present with these key symptoms: Flank pain that can radiate to the groin Hematuria (blood in urine) - either visible or microscopic Possible complications include urinary obstruction with decreased or absent urine output, particularly in patients with a single functioning kidney or pre-existing renal disease TABLE 16–12 Common mechanical causes of urinary tract obstruction. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 13 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Etiology Calcium is the most common component of renal stones, found in at least 75% of cases. The main causes of calcium stones are: Idiopathic hypercalciuria (most common) Hyperuricosuria Hyperparathyroidism TABLE 16–13 Major causes of renal stones. Pathology & Pathogenesis Renal stone formation and its risk factors: Basic Mechanism: Renal stones form when substances in urine become less soluble, leading to salt precipitation. https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 14 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM Risk Factors: Dehydration - maintaining 2L daily urine output is protective High-protein diet - causes metabolic acidosis and affects calcium metabolism High sodium intake - increases calcium excretion and stone formation Stone formation per se within the renal pelvis is painless until a fragment breaks off and travels down the ureter, precipitating ureteral colic. Hematuria and renal damage can occur in the absence of pain. Clinical Manifestations Pain occurs due to distention of the ureter, renal pelvis, or renal capsule While symptoms like pain, hematuria, and ureteral obstruction are typically temporary, major complications can include: 1. Hydronephrosis and potential permanent renal damage from complete obstruction 2. Infection or abscess formation behind obstructing stones 3. Renal damage from repeated stones 4. Hypertension due to increased renin production CHECKPOINT 17. How do patients with renal stones present? 18. Why do renal stones form? 19. What are the common categories of renal stones (by composition)? CASE STUDIES Yeong Kwok, MD (See Chapter 25, p. 775–76 for answers) CASE 84 A healthy 26-year-old woman sustained a significant crush injury to her right upper extremity while on the job at a local construction site. She was brought to the emergency department and subsequently underwent pinning and reconstructive surgery and received perioperative broad-spectrum antibiotics. Her blood pressure remained normal throughout her hospital course. On the second hospital day, a medical consultant noted a marked increase in her creatinine, from 0.8 to 1.9 mg/dL. Her urine output dropped to 20 mL/h. Serum creatine kinase was ordered and reported as 3400 units/L. Questions A. What are the primary causes of this patient’s acute kidney injury? How should her kidney injury be categorized (as prerenal, intrarenal, or postrenal)? B. Which two types are most likely in this patient? How might they be distinguished clinically? C. How should the patient be treated? CASE 85 A 58-year-old obese woman with hypertension, type 2 diabetes, and chronic kidney disease is admitted to hospital after a right femoral neck fracture sustained in a fall. Recently, she had been complaining of fatigue and was started on epoetin alfa subcutaneous injections. Her other medications include an angiotensin-converting enzyme inhibitor, a β-blocker, a diuretic, calcium supplementation, and insulin. On review of systems, she reports mild tingling in her lower extremities. On examination, her blood pressure is 148/60 mm Hg. She is oriented and able to answer questions appropriately. There is no evidence of jugular venous distention or pericardial friction rub. Her lungs are clear, and her right lower extremity is in Buck traction in preparation for surgery. Asterixis is absent. Questions A. Describe the pathogenesis of bone disease in chronic kidney disease. How could this explain the patient’s increased likelihood of sustaining a fracture after a fall? B. Why was erythropoietin therapy initiated? https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 15 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM C. What is the significance of a pericardial friction rub in the setting of chronic kidney disease? CASE 86 A 28-year-old nursery school teacher developed a marked change in the color of her urine (“cola-colored”) 1 week after she contracted impetigo from one of her students. She also complained of a new onset of global headaches and fluid retention in her legs. Examination revealed a blood pressure of 158/92 mm Hg, resolving honey-crusted pustules over her right face and neck, 1+ pitting edema of her ankles, and no cardiac murmur. Urinalysis revealed 2+ protein and numerous red cells and red cell casts. Her serum creatinine was elevated at 1.9 mg/dL. Serum complement levels (CH50, C3, and C4) were low. She was diagnosed with poststreptococcal glomerulonephritis. Questions A. What is the relationship between the patient’s skin infection and the subsequent development of glomerulonephritis? B. Describe the pathogenesis of this disorder. C. What is the natural history of this form of immune complex vasculitis? CASE 87 A 40-year-old man with Hodgkin lymphoma is admitted to the hospital because of anasarca. He has no known history of renal, liver, or cardiac disease. His serum creatinine level is slightly elevated at 1.4 mg/dL. His serum albumin level is 2.8 g/dL. Liver function test results are normal. Urinalysis demonstrates no red or white blood cell casts, but 3+ protein is noted and a 24-hour urine collection shows a protein excretion of 4 g/24 h. He is diagnosed with nephrotic syndrome, and renal biopsy suggests minimal-change disease. Steroids and diuretics are instituted, with gradual improvement of edema. The hospital course is complicated by deep venous thrombosis of the left calf and thigh that requires anticoagulation. Questions A. This patient suffers from generalized body edema (anasarca). By what mechanism does the edema form? B. What are the characteristic morphologic features seen in minimal-change disease? How does this differ from other forms of glomerulonephritis? C. How does nephrotic syndrome predispose this patient to thromboembolic disease? CASE 88 A 48-year-old white man presents to the emergency department with unremitting right flank pain. He denies dysuria and fever. He reports significant nausea without vomiting. He has never experienced anything like this before. On examination, he is afebrile, and his blood pressure is 160/80 mm Hg with a pulse rate of 110/min. He is writhing on the gurney, unable to find a comfortable position. His right flank is mildly tender to palpation, and abdominal examination is benign. Urinalysis is significant for 1+ blood, and microscopy reveals 10–20 red blood cells per high-power field. Nephrolithiasis is suspected, and the patient is intravenously hydrated and given pain medication with temporary relief. Questions A. What is the most likely cause of this patient’s renal stone disease? B. Describe your discharge instructions to the patient, reflecting on the pathogenesis of stone disease. C. Why is this disorder painful? https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 16 of 17 (1) Hammer Ch. 16 HIGHLIGHTS ONLY SUMMARIZED 1/29/25, 4:33 PM https://www.notion.so/Hammer-Ch-16-HIGHLIGHTS-ONLY-SUMMARIZED-188cbd87b68480b59edff8069bcd2fd6 Page 17 of 17