Nephrology Flashcards

Question

diabetic nephropathy

Answer 1

Proteinuria is an independent predictor of cardiovascular risk in patients with diabetes mellitus and/or hypertension. Screening for proteinuria by performing a spot urine albumin:creatinine ratio is the most commonly performed investigation to assess this risk. From a pathophysiological perspective, albuminuria reflects glomerular protein leak, whereas proteinuria more broadly reflects protein excretion into the urine from anywhere along the nephron. Additionally, a urine albumin:creatinine ratio is more sensitive than a urine protein:creatinine ratio for detecting low levels of proteinuria (e.g. negative or protein 1+ on reagent strip urinalysis) and is the NICE recommended method for screening for diabetic nephropathy. This makes urine albumin:creatinine ratio a better option than protein:creatinine ratio. A 24-h urine collection is more cumbersome for patients to perform and, as they are commonly incompletely performed, are often not accurate. Urinary lipid peroxide is a potential biomarker to assess oxidative stress. It is not routinely used in clinical practice and is obviously incorrect. Urine microscopy will not give information on proteinuria.

Answer 2

X-linked: The most common form (around 85%), - early childhood & ESKD by 40 Autosomal recessive (early childhood & ESKD by 30 ), Autosomal dominant (present late in life after 40), Autosomal digenic Mutations in type IV collagen, a protein vital for the structure of the glomerular basement membrane in the kidneys. Kidney problems: Progressive kidney disease: Kidney function declines over time, potentially leading to ESKD Proteinuria, Hematuria Hearing loss: Progressive sensorineural hearing loss, often starting in childhood or early adolescence. Eye abnormalities: Anterior lenticonus, Maculopathy Corneal endothelial vesicles. Other potential complications: Hypertension, smooth muscle tumors (leiomyomas).

Answer 3

75 % idiopethic PLA2R antibodies - primary membranous nephropathy primarily caused by the formation of immune complexes that bind to antigens in the glomerulus, activating the complement system and damaging the glomerular cells. manifesting as nephrotic syndrome - edema (swelling), weight gain, and foamy urine due to proteinuria. And fatigue, high blood pressure, and cholesterol level changes. Or asymptomatic Diagnosis: Involves thickening of the glomerular basement membrane, often with the presence of immune complexes (antibodies) along the subepithelial region of the glomeruli.

Answer 4

This patient has nephrotic syndrome (characterised by the triad of oedema, proteinuria (>3g/24h) and hypoalbuminaemia). Of the options listed, minimal change disease is the most likely cause of nephrotic syndrome in this patient. A trigger, such as a viral respiratory tract infection, can occur before the acute presentation. IgA nephropathy and membranoproliferative glomerulonephritis can present with nephrotic syndrome, although these diseases much more commonly present with progressive renal impairment and haematuria with non-nephrotic proteinuria. Minimal change disease is a much more common cause of nephrotic syndrome than these disorders. Autosomal dominant polycystic kidney disease and Alport syndrome are respectively, the first and second, most common hereditary kidney diseases. They are not causes of nephrotic syndrome and so are not correct options.

Answer 5

caused by the deposition of IgA immune complexes in the glomeruli, the filtering units of the kidneys. This deposition triggers inflammation and damage, leading to kidney dysfunction Abnormal IgA1: Patients with IgAN have increased levels of circulating IgA1 with a specific type of abnormal glycosylation (O-glycosylation) where galactose is deficient. This aberrant glycosylation makes the IgA1 more susceptible to antibody recognition. Autoantibodies - gG and IgA antibodies that are specific to the galactose-deficient IgA1. visible or microscopic hematuria (blood in the urine), proteinuria (protein in the urine), and occasionally swelling (edema), high blood pressure, or fatigue or Asymptomatic

Answer 6

impaired 1-alpha hydroxylation of 25-hydroxycholecalciferol by the kidney to 1,25-dihydroxycholecalciferol. 1,25-dihydroxycholecalciferol is the active form of vitamin D. In health, 1,25-dihydroxycholecalciferol promotes calcium and phosphate absorption from the gut and kidney, suppresses parathyroid hormone secretion and acts on the bone to stimulate osteoclast activity. The deficiency of 1,25-dihydroxycholecalciferol observed in chronic kidney disease therefore explains the low serum calcium measurement observed in this patient. Phosphate levels are raised in chronic kidney disease due to impaired renal excretion. The combination of low calcium and raised phosphate then leads to elevated parathyroid hormone levels which causes increased bone turnover and raised serum alkaline phosphatase levels.

Answer 7

to damaged kidney filters (glomeruli), leading to excessive protein (primarily albumin) leaking into the urine. Damaged Glomeruli Protein Loss and Hypoalbuminemia Edema Hyperlipidemia Proteinuria greater than 3-3.5 g/24 hour or spot urine protein:creatinine ratio of >300-350 mg/mmol. Serum albumin <25 g/l. Clinical evidence of peripheral oedema. Severe hyperlipidaemia (total cholesterol often >10 mmol/l) is often present. Treatment - Minimal change disease: Steroid medication is often effective. Other causes: Treatment may involve immunosuppressants, ACE inhibitors, ARBs, and other medications as needed.

Answer 8

Key Characteristics of dRTA: Inability to excrete acid: The kidneys cannot effectively remove hydrogen ions (H+) from the blood and into the urine, even when the body is acidic. Alkaline urine: above 5.5). Hypokalemia Hypercalciuria: kidney stones. Nephrolithiasis low urinary amonium decreased urinary citrate Nephrocalcinosis: Bone disease: In untreated cases, particularly in children, it can lead to rickets or osteomalacia due to calcium and phosphate loss from bone. Metabolic acidosis Treatment: Oral alkali therapy, Potassium supplementation Diuretics Mutations in genes like ATP6V0A4 and ATP6V1B1, which encode proteins involved in the H+ ATPase pump (a proton pump), autosomal dominant or autosomal recessive pattern.

Answer 9

ccurs in individuals with advanced liver disease, often cirrhosis. It's distinct from other causes of AKI, as it's primarily due to reduced blood flow to the kidneys caused by liver failure. rapid decline in kidney function, leading to a decrease in urine output (oliguria) and a build-up of fluids in the body.

Answer 10

Causes: Common causes include: 1. Ischemia: Lack of blood flow and oxygen to the kidneys, often due to low blood pressure, shock, or dehydration. hypovolemia hypotension, or systemic or local hypoperfusion. Tubular Cell Injury: The kidneys, especially the tubule cells, are vulnerable to ischemia due to their high metabolic demands. Cell Death:necrosis in the tubules, disrupting their function. Reperfusion Injury: When blood flow is restored after a period of ischemia, a process called reperfusion injury can further damage the kidneys. Clinical Presentation: Oliguria: Muddy Brown Casts: These are granular casts containing cellular debris and are a hallmark of ATN in urine. Elevated Creatinine and Urea: These waste products build up in the blood due to impaired kidney function. 2. Nephrotoxins: aminoglycocides, gentamicin, vancomycin, Exposure to certain drugs or toxins that can damage the kidney tubules. exposure to certain substances directly damages the renal tubular epithelial cells, leading to their death and dysfunction Initial Insult: Nephrotoxic agents, such as certain antibiotics (aminoglycosides), contrast dyes, and heavy metals, directly interact with and damage the renal tubular epithelial cells. 2. Tubular Damage: This initial insult leads to a cascade of events, including inflammation, oxidative stress, and the release of pro-inflammatory cytokines, further contributing to tubular cell injury. 3. Cell Death and Necrosis: The damaged cells undergo necrosis (cell death), resulting in the formation of casts (cellular debris) within the tubules. 4. Tubular Dysfunction: The damaged tubules are unable to effectively reabsorb water, electrolytes, and other substances from the filtrate, leading to impaired kidney function and decreased urine output. 5. Intratubular Obstruction: The cellular debris and casts can obstruct the tubules, further impairing fluid flow and contributing to the development of acute kidney injury. 6. Renal Vasoconstriction: Some nephrotoxins can also induce renal vasoconstriction, further reducing blood flow to the kidneys and exacerbating the injury. decreased urine, Elevated Creatinine and Urea, a rise in serum creatinine and/or decreased urine output, along with urinalysis revealing muddy brown casts, which are characteristic of ATN. Sepsis: A severe infection can lead to reduced blood flow and kidney damage.

Answer 11

Prerenal azotemia: In prerenal azotemia, the kidneys are not directly damaged, but renal blood flow is reduced due to volume depletion or other factors. Urinalysis: Prerenal azotemia typically shows normal or hyaline casts, while ATN shows muddy brown casts. Response to Fluid Replenishment: Prerenal azotemia often improves with fluid repletion, whereas ATN usually does not respond to fluid repletion alone. FENa and Urea: FENa and fractional excretion of urea may be lower in prerenal azotemia compared to ATN.

Answer 12

pproximately 40% of patients with CSS may test positive for ANCAs, most commonly perinuclear ANCAs (pANCAs) targeting myeloperoxidase (MPO). C Triad - asthma, hypereosinophilia, and necrotizing vasculitis. Asthma, Allergic Rhinitis, Sinusitis, Eosinophilia Skin Manifestations: Rash, skin nodules, purpura, and petechiae. - 3-9 years of progression , <65 Neuropathy, Gastrointestinal Involvement Fatigue, Fever, and Weight Loss, Joint and Muscle Pain: Stages - Prodromal Phase: Characterized by allergic symptoms like asthma, rhinitis, and sinusitis. Eosinophilic Phase: Marked by peripheral blood eosinophilia and eosinophilic infiltrates in tissues, particularly the lungs, myocardium, and gastrointestinal tract. Vasculitic Phase: Systemic vasculitis affecting various organs, potentially leading to severe organ damage. Lungs: Pulmonary hemorrhage, pneumonia-like symptoms, and damage to the blood vessels in the lungs. Heart: Pericarditis, myocarditis, and heart failure. - major cause of death Kidneys: Glomerulonephritis, potentially leading to kidney failure. Peripheral nerves: Neuropathy, causing numbness, tingling, and weakness.

Answer 13

a hyperkalemic form of RTA characterized by (normal anion gap)hyperchloremic metabolic acidosis, often associated with hypoaldosteronism,hypo-renin due to reduced aldosterone action, leading to hyperkalemia and a normal anion gap metabolic acidosis. Impaired Aldosterone Action: Reduced Hydrogen Ion Secretion: Impaired Ammonia Production: Reduced Ammonium Excretion: Hyperkalemia and Metabolic Acidosis: Low Urinary pH: Causes of Type 4 RTA: Aldosterone deficiency: primary adrenal insufficiency, hyporeninemic hypoaldosteronism (a common cause in chronic kidney disease), and certain medications. Aldosterone resistance: Medications: Some medications, including ACE inhibitors, ARBs, certain diuretics, and NSAIDs, can contribute to hyperkalemia and, potentially, type 4 RTA. Underlying diseases: diabetic nephropathy. Treatment focuses on addressing the underlying cause of the hyperkalemia and acidosis, which may include: Mineralocorticoid replacement therapy: Fludrocortisone Dietary potassium restriction: Diuretics: Bicarbonate supplementation:

Answer 14

kidney damage caused by the backward flow of urine (reflux) from the bladder into the kidneys. This condition, often linked to vesicoureteral reflux (VUR), can lead to scarring, kidney infections (acute pyelonephritis), and potentially high blood pressure or kidney failure. Imaging Tests: Renal Ultrasound: swollen kidneys or other structural abnormalities. Voiding Cystourethrogram (VCUG): This X-ray procedure uses contrast dye to visualize the bladder and ureters while the patient is urinating, revealing the presence and degree of reflux. Renal DMSA Scan: A nuclear medicine scan using a radioactive tracer that accumulates in healthy kidney tissue, highlighting any areas of scarring caused by reflux. Radionuclide Cystogram (RNC): A nuclear scan similar to VCUG, but with less radiation exposure, used to assess reflux.

Answer 15

complication of systemic lupus erythematosus (SLE) Blood in the urine, Foamy urine, Swelling (edema), High blood pressure: capilary wire looping Antibodies against double-stranded DNA (anti-dsDNA), which form immune complexes that deposit in the kidney. These deposits trigger an inflammatory response, damaging the glomeruli, the filtering units of the kidneys.

Answer 16

Hyperacute Rejection: within minutes to hours after transplantation. It's caused by pre-existing antibodies in the recipient's blood that recognize and attack the donor kidney. These antibodies, typically against ABO blood group or HLA antigens, trigger inflammation and damage to the graft vessels, leading to immediate graft failure. Acute Rejection: within weeks to months after transplantation and is primarily driven by T-cell-mediated immunity. involve the tubulointerstitial (T-cells attacking the tubules and surrounding tissues) or arterial components (T-cell attack on the arteries). Antiviral - cytomegalovirus (CMV) and other herpesviruses, Valganciclovir, intravenous ganciclovir, and high-dose valacyclovir. Immunosuppressants: Tacrolimus, Mycophenolate, and Prednisolone are commonly used immunosuppressants, requiring careful monitoring and dose adjustments. Trimethoprim-sulfamethoxazole (TMP-SMX) is commonly used for prophylaxis against Pneumocystis pneumonia and other infections, while other antibiotics like cefazolin or ampicillin-sulbactam may be used for specific surgical-site infections. Chronic Rejection: long-term process characterized by gradual loss of graft function over months to years. It's thought to be a combination of ongoing immune responses, ischemia-reperfusion injury, and the effects of immunosuppressant medications. Chronic rejection leads to fibrosis and scarring in the graft, ultimately impairing its ability to function properly. igG

Answer 17

inhibiting the enzyme inosine monophosphate dehydrogenase (IMPDH) his inhibition leads to a depletion of guanine nucleotides in T and B cells, disrupting their DNA synthesis and ultimately suppressing cell-mediated immune responses and antibody formation. immunosuppressant in solid organ transplantation to prevent or treat acute and chronic rejection

Answer 18

Alcohol-related cirrhosis: A history of excessive alcohol consumption in the absence of other causes of cirrhosis is a significant factor in diagnosis. Primary biliary cirrhosis: This autoimmune liver disease is often diagnosed based on persistently elevated alkaline phosphatase levels, presence of anti-mitochondrial antibodies, and liver histology consistent with the disease. Decompensated Cirrhosis: Signs of decompensated cirrhosis include ascites, jaundice, and hepatic encephalopathy. risk factors like increased alcohol intake, hepatitis B or C infection, obesity, type 2 diabetes, autoimmune liver disease, or exposure to certain medications.

Answer 19

Types of Renal Tubular Acidosis: Distal RTA (Type 1): common Proximal RTA (Type 2): This type involves the inability of the kidneys to reabsorb bicarbonate ions (buffers) from the urine back into the blood. It is often associated with Fanconi syndrome and can be inherited or acquired. Primary defect: Kidneys fail to reabsorb bicarbonate (HCO3-) in the proximal tubules, leading to a loss of bicarbonate in the urine and a build-up of acid in the blood. Symptoms: Similar to Type 1 RTA, with muscle weakness, fatigue, and bone problems. Hyperkalemic RTA (Type 4): Mixed RTA (Type 3): This rare type involves defects in both proximal and distal tubules, resulting in impaired bicarbonate reabsorption and hydrogen ion excretion. Primary defect: A defect affecting both bicarbonate reabsorption (proximal) and acid excretion (distal). Symptoms: Combination of symptoms from Type 1 and Type 2 RTA, including muscle weakness, fatigue, kidney stones, bone problems, and potential hearing loss.

Answer 20

a rare neurological condition where abnormal amyloid proteins accumulate in peripheral nerves, causing damage and dysfunction. This can lead to a range of symptoms, including pain, numbness, tingling, and autonomic dysfunction causes Amyloidosis: AL Amyloidosis: Familial Amyloid Polyneuropathy (FAP): A group of hereditary disorders caused by mutations in genes that produce amyloid proteins like transthyretin (ATTR-PN). Key diagnostic tools include nerve conduction studies, skin biopsies, and potentially genetic testing in cases of familial amyloidosis. Peripheral Neuropathy: Pain, Altered Sensations, Weakness, Autonomic Neuropathy, Digestive Issues, Orthostatic Hypotension, Sweating Abnormalities, Sexual Dysfunction, Balance Problems, Carpal Tunnel Syndrome: Renal Manifestations: Proteinuria, Nephrotic Syndrome, Kidney Impairment Amyloid deposits can be found in the glomeruli, blood vessels, and interstitial tissues.

Answer 21

ADPKD: The most common type, ADPKD, is caused by mutations in the PKD1 or PKD2 genes, which produce proteins called polycystin-1 and polycystin-2. ARPKD: A rarer form, ARPKD, is caused by mutations in the PKHD1 gene involves defects in the structures and functions of the kidneys' tubules and the cilia within them, ultimately causing abnormal cell growth and fluid accumulation in the cysts. flank pain, blood in the urine, and high blood pressure. Other potential complications include liver cysts, urinary tract infections, and kidney stones. In autosomal dominant PKD (ADPKD), cysts can also develop in the liver, pancreas, and other organs. increased risk of brain aneurysms and heart valve abnormalities. chrom 16, 4

Answer 22

Reduced Erythropoietin (EPO) Production: The kidneys are the primary source of EPO, which signals the bone marrow to produce red blood cells. When kidneys are damaged, they produce less EPO, leading to fewer red blood cells and anemia. Other Factors: In addition to EPO deficiency, other factors can contribute to anemia in CKD, including iron deficiency, inflammation, and reduced red blood cell lifespan. Iron Deficiency: diagnose anemia, including checking hemoglobin levels, red blood cell count, and iron levels. B12 should be corrected Treatment Options: Erythropoiesis-Stimulating Agents (ESAs) Iron Supplements Blood Transfusions Addressing Underlying Conditions

Answer 23

decline in kidney function, or acute kidney injury (AKI), that occurs after exposure to contrast agents used in medical imaging procedure CIN is typically defined as a rise in serum creatinine of 0.5 mg/dL or more, or a 25% increase from baseline within 48-72 hours after contrast exposure. Risk Factors: Pre-existing kidney disease, diabetes, heart disease, and the use of certain medications

Answer 24

GPA's renal involvement involves inflammation and damage to the glomeruli due to necrotizing vasculitis and granuloma formation, leading to glomerulonephritis and potentially kidney failure. Vasculitis: inflammation affects small to medium-sized vessels, including those in the kidneys. Glomerulonephritis: Necrotizing vasculitis: where the inflammation causes tissue damage and necrosis (tissue death). This tissue damage can further impair kidney function. Granuloma formation: In GPA, granulomas, inflamed masses of cells, can form in the kidneys and other organs. These granulomas can further obstruct blood flow and cause damage to the surrounding tissues. ANCA antibodies: PR3 Progression to kidney failure, poor prognosis - Adverse events cardiovascular disease, and malignancy, early AKI, Early severe forms of GPA, Older patients

Answer 25

characterized by significant proteinuria due to podocyte damage, but the exact cause is unknown. It's thought to involve a combination of immunologic dysregulation and podocyte injury, potentially leading to the leakage of protein into the urine. While T-cell dysfunction and cytokine release are implicated, the specific mechanisms and factors involved are still being investigated. Kidney disorder characterized by proteinuria, the glomeruli (the filtering units of the kidney) appear normal or nearly normal under light microscopy,

Answer 26

Gout, caused by high uric acid levels, can lead to kidney disease, and kidney disease, including nephrotic syndrome, can also cause elevated uric acid. Additionally, nephrotic syndrome can lead to protein loss in urine, which can affect overall health and potentially contribute to kidney damage.

Answer 27

Pregnancy Active Anticoagulation Severe or Uncontrolled Hypertension Aortic Aneurysms Uncorrected Bleeding Disorders (Coagulopathies): Untreated Urinary Tract Infections Severe Skeletal Abnormalities (like Scoliosis):

Answer 28

cute vs. Chronic: Interstitial nephritis can be either acute, meaning it develops quickly and may be caused by drug reactions or infections, or chronic, meaning it develops over a longer period and may have various underlying causes Usually drug-induced with >250 known triggering medications. Common classes include beta-lactam and fluoroquinolone antibiotics, proton-pump inhibitors, non-steroidal anti-inflammatory drugs (NSAIDs), and immune checkpoint inhibitors. Also occurs in inflammatory diseases such as sarcoidosis, Sjogren syndrome, IgG4-related diseases, and tubulo-interstitial nephritis with uveitis (TINU) syndrome. Various infectious agents (viruses, bacteria, fungi) and some malignancies can also cause AIN

Answer 29

condition caused by excessive intake of calcium and absorbable alkali, leading to hypercalcemia, metabolic alkalosis, and kidney impairment. It's often associated with consuming large amounts of calcium supplements, particularly calcium carbonate, or antacids containing calcium Hypercalcemia: High calcium levels in the blood. Metabolic alkalosis: A shift in the body's acid-base balance toward alkaline, often due to increased bicarbonate retention. Renal impairment: Causes: Calcium supplements: Excessive intake of calcium carbonate, often taken to prevent osteoporosis. Antacids:

Answer 30

can cause both proximal and distal renal tubular acidosis (RTA), including Fanconi's syndrome Renal Tubular Acidosis: RTA, a type of renal tubular dysfunction, occurs when the kidneys are unable to effectively excrete excess acid in the urine, leading to metabolic acidosis. In Wilson's disease, both proximal and distal RTA can occur. Distal RTA and Bone Disease: Distal RTA can impair the body's ability to absorb and utilize calcium and phosphate, which are crucial for bone health. This can lead to vitamin D-resistant rickets, osteomalacia, and other metabolic bone diseases. Fanconi's Syndrome: A specific type of proximal RTA, Fanconi's syndrome, is also associated with Wilson's disease. It involves a wider range of defects in tubular function, including the inability to reabsorb various substances like glucose, amino acids, and phosphate.

Answer 31

Retroperitoneal fibrosis (RPF)

Answer 32

Common crystals: Calcium oxalate- PTH,, uric acid, and Calcium/triple phosphate crystals - Alkaline urine are frequently seen in urine, even in healthy individuals. Less common crystals: Cystine crystals (associated with cystinuria) - hexaganal, CNnitroprasie positive tyrosine crystals (linked to liver disease or tyrosinemia), and leucine crystals (seen in severe liver disease or maple syrup urine disease) are less common but can be significant. uric acid - romboid crystals Drug-induced crystals: Certain medications can cause crystals to form in the urine.

Answer 33

Proteinuria: Protein in the urine, a sign of damage to the kidney filters. Edema: Swelling, particularly in the face, legs, and ankles, due to fluid buildup. High blood pressure (hypertension): MCGN can sometimes lead to elevated blood pressure. Hematuria: Blood in the urine. Kidney function decline Complement Regulatory Proteins: factor H (CFH), factor I (CFI), and membrane cofactor protein (MCP) C3 Nephritic Factor (C3NeF) C3 and LMNA

Answer 34

Key features of RPGN: Rapid decline in kidney function: This is a hallmark of RPGN, with the decline occurring over a relatively short period. Nephritic syndrome: hematuria, proteinuria, and decreased urine output (oliguria or anuria). Glomerular crescent formation: Crescent formation is a characteristic histologic finding, indicating severe glomerular injury. progression to end-stage kidney disease: Without timely treatment, RPGN can lead to irreversible kidney damage and necessitate dialysis or a kidney transplant. This condition is primarily defined by the presence of extensive glomerular crescents, which are scars in the kidney glomeruli, seen in biopsies. Causes and types of RPGN: infections, immune disorders, and vasculitis. Classification: RPGN is classified based on the type of immune complex deposition, linear antibody deposition, or pauci-immune disorders. Anti-GBM disease: antibodies against the glomerular basement membrane, a common cause of RPGN Immune complex glomerulonephritis: immune complexes depositing in the glomeruli. Pauci-immune glomerulonephritis: This type lacks significant immune complex deposits, often associated with ANCA-associated vasculitis. Treatment: immunosuppressants like glucocorticoids, cyclophosphamide, or rituximab, plasma exchange

Answer 35

Class I: Minimal mesangial lupus nephritis: Involves minimal immune complex deposits in the mesangium, a region within the glomerulus. Class II: Mesangial proliferative lupus nephritis: Characterized by mesangial hypercellularity (increased mesangial cells) and immune complex deposits. Class III: Focal lupus nephritis: Involves less than 50% of glomeruli with endocapillary and/or extracapillary proliferation, often with segmental involvement. Class IV: Diffuse lupus nephritis: Affects 50% or more of glomeruli with diffuse endocapillary and/or extracapillary changes, which can be segmental or global. Class V: Membranous lupus nephritis: Defined by subepithelial immune complex deposits, often associated with nephrotic syndrome. Class VI: Advanced sclerosing lupus nephritis: Represents advanced chronic disease with extensive glomerulosclerosis (scarring of the glomeruli).

Answer 36

Congenital Nature Cystic Dilatation: Sponge-like Appearance: The cysts give the kidney's medulla (inner region) a sponge-like appearance, Bilateral or Unilateral Asymptomatic in Many Potential Complications: While benign in many cases, MSK can lead to complications such as: Kidney Stones: Urinary Tract Infections: Nephrocalcinosis: