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Mutravah rog
- 1. A Compilation on maU~vah s~aotsagat raoga PRESENTED BY : Gurkirat Kaur DEPARTMENT OF ROG NIDANA DAYANAND AYURVEDIC COLLEGE , JALANDHAR
- 2. maU~vahs~aotaoduiYT maU~vahs~aotsa ka maUla : • Aacaaya- cark matanausaar maU~vahs~aotsa ka maUla baist hO. • Aacaaya- sauEaut matanausaar maU~vahs~aotsa ka maUla baist , maoZ/ hO. maU~vahs~aotaoduiYT ko karNa : maUi~taodkBaxyas~IsaovanaanmaU~inaga`hat I maU~vaahIina duYyaint xaINasyaaiBaxatsya ca II ( ca. iva. 5 /19) • maU~ ka vaoga raokkr jala pInao sao • Baaojana krnao sao • s~Ip`saMga krnao sao • maU~ ko vaoga kao raoknao sao • SarIr ko AiQak xaINa haonao sao • maU~vah s~aotsa pr AaGaat laganao sao yaa xat hao jaanao sao maU~vah s~aotsa dUiYat hao jaata hO.
- 3. maU~vahs~aaotaoduiYT ko laxaNa : [ ca .iva. 5/ 6 (5)] maU~vahs~aotsa ko dUiYat haonao pr ivaSaoYa laxaNa ]%pnna haoto hOM.jaOsao ik • maU~ ka AiQak inaklanaa • maU~ ka $k $k kr Aanaa • dUiYat maU~ Aanaa • baar baar qaaoDa qaaoDa dd- ko saaqa maU~%yaaga krnaa - [na laxaNaaoM kao doKkr ]sa raogaI ko maU~vah s~aotsa kao dUiYat samaJanaa caaihe.
- 4. maU~raoga ko $p ( A.).ina. 9) maU~aitp`vaRit janya maU~raoga maU~p`vaRit janya raoga
- 5. maU~kRcC/ maU~sya kRcC/oNa mahta du:KoNa p`vaRit:. maQaukaoSa maU~ kI kYTp`d p`vaRit kao hI maU~kRcC/ khto hOM. Aqaa-t raogaI kao maU~ A%yant kYT ko saaqa baUMd baUMd krko ]trta hO.yah baist ka raoga haota hO.[samaoM maU~inamaa-Na kI p`ik`yaa maoM kao[- vyavaQaana nahIM haota yah inarntr calatI rhtI hO AaOr maU~ sao baist pirpUNa- rhta hO maU~ao%saga- kI [cCa BaI haotI hO laoikna maU~maaga- maoM iksaI p`kar ko AvaraoQa yaa ivakar ko ]%pnna hao jaanao ko karNa maU~%yaaga maoM kYT haota hO evaM samyak $p sao maU~ao%saga- nahIM haokr baUMd baUMd krko ]trta hO. inadana ( ca. ica. 26 /32) • A%yaaiQak vyaayaama • A%yaaiQak toja calanao vaalaI savaarI • tIxNa AaOYaiQa • $xa pdaqa- • A%yaaiQak maVpana • AjaINa- • AQyaSana • Aagantuja karNa
- 6. samp`aiPt ( ca. ica . 26 /33) Apnao Apnao karNaaoM sao p`kuipt vaataid daoYa pRqak pRqak Aqavaa ek saaqa baist maoM phuMca kr jaba saMkaoca yaa xaaoBa ]%pnna krto hOM tba maU~ %yaaga krto samaya raogaI kao kYT haota hO. yahI maU~kRcC/ hO. inadana saovana vaatid daoYa p`kaop baist maU~maaga- maoM xaaoBamaU~kRcC/ daoYa dUYya AiQaYzana • daoYa - i~daoYa , vaatp`Qaana • dUYya - maU~ , jala • AiQaYzana - baist , maU~maaga-
- 7. maU~kRcC/ ko p`kar vaaitk pOitk kfja sainnapatja AiBaGaatja / r>ja SakRt janya ASmarIja Sauk`ja
- 8. laxaNa : o saamaanya laxaNa :- • qaaoDa qaaoDa baar baar kYT ko saaqa maU~%yaaga o ivaSaoYa laxaNa :- • vaaitk maU~kRcC - vaMxaNa baistp`doSa maoZ/ maoM AittIva` pIDa tqaa qaaoDI qaaoDI maa~a maoM baar baar maU~ %yaaga haonaa vaaitk maU~kRcC/ ka laxaNa hO. • pOitk maU~kRcC/ - kRcC/ta ko saaqa baar baar pItvaNa- sar@t sa$ja sadah maU~%yaaga haonaa pOitk maU~kRcC/ ka laxaNa hO. • kfja maU~kRcC/ - baist tqaa ilaMga maoM Saaoqa gau$%va ko saaqa maU~ maoM ipicClata kfja maU~kRcC/ ko laxaNa hOM. • sainnapatja maU~kRcC/ - ]prao> saBaI laxaNa hao sakto hOM. • AiBaGaatja maU~kRcC/ - maU~vaahI s~aotaoM maoM AaByantr Salya Aqavaa baa( AiBaGaat laganao sao jaao BayaMkr maU~kRcC/ ]%pnna haota hO. • SakRt janya maU~kRcC/ - purIYa ko vaoga kao raoknao sao malavaayau ivalaaoma haokr ]dr maoM AaQmaana vaaitk SaUla tqaa maU~avaraoQa ]%pnna kr dota hO. • ASmarIja maU~kRcC - maU~aSmarI ko karNa haonao vaalaa maU~kRcC/ ASmarIja maU~kRcC/ khlaata hO. [sako karNa h%pIDa kmpna kuixaSaUla AignamaaMV maUcCa- tqaa BayaMkr maU~kRcC/ haota hO. • Sauk`ja maU~kRcC/ - Apnao sqaana sao cyaut huAa Sauk` jaba daoYaaoM ko p`kaop sao Ava$Qa haokr maU~maaga- maoM $k jaata hO tba raogaI kao saSauk` maU~ %yaaga haota hO tqaa baist evaM maoZ/ maoM pIDa haotI hO.
- 9. maU~aGaat yah BaI maU~kRcC/ sao saamya rKta huAa maU~vah s~aotaogat vyaaiQa hO.[sa vyaaiQa maoM BaI $k $k kr qaaoDa qaaoDa AaOr kYT ko saaqa maU~ao%saga- haota hO.[samaoM AaOr maU~kRcC maoM yah hI Antr hO ik ]samaoM maU~ ]trta tao hO laoikna baUMd baUMd krko baDI kiznaa[- ko saaqa jaba ik maU~inamaa-Na barabar haota rhta hO AaOr maU~aSaya maU~ sao Bara rhta hO. laaoikna maU~aGaat maoM [sako ivaprIt maU~ao%saga- haota hI nahIM hO Aqaa-t vaR@kaoM maoM hI maU~inamaa-Na kI p`ik`yaa baaiQat haokr maU~inamaa-Na band hao jaata hO. inadana ( ma. ina . 31 /1 maQaukaoSa vyaa#yaa) purIYa Sauk` Aaid vaogaavaraoQa evaM $xa pdaqaao-M ka Aitsaovana samp`aiPt inadana saovana vaatp`Qaana daoYa p`kaop maU~aGaat
- 10. daoYa dUYya AiQaYzana • daoYa - i~daoYa vaatp`Qaana • dUYya - maU~ • AiQaYzana - baist saamaanya laxaNa • [sa raoga maoM maU~ ka AvaraoQa ivaSaoYata haota hO.ikntu saaqa maoM kRcC/ BaI Alp maa~a maoM haota hO. Baod • Aacaaya- cark - 13 p`kar • Aacaaya- sauEaut - 12 p`kar • Aacaaya- vaagBaT - 20 p`kar 4 p`kar kI ASmarI 4 p`kar ka maU~kRcC/ evaM 12 p`kar ko maU~aGaat ka vaNa-na ikyaa hO.
- 11. maU~Gaat ko P`akar vaatkuilaka vaatvaist maU~ao%saMga maU~ jazr maU~atIt vaistkuNDla AYzIlaa maU~ ga`inqa ]YNavaat maU~Sauk` ivaDivaGaat maU~saad maU~xaya
- 12. vaatkuNDilaka vaatla Aahar ivahar tqaa vaoga ivaQaarNa ko karNa p`kuipt vaistgat vaayau maU~ maoM p`ivaYT haokr kuNDlaIkRt haokr saMcaar krta hO.ijasako pirNaama sva$p baist maoM pIDa tqaa qaaoDI qaaoDI maa~a maoM baar baar sakYT maU~%yaaga haota hO. vaatvaist maU~vaoga kao raoknao ko karNa vaist maoM p`kuipt huAa vaayau maU~avaraoQa vaodnaa evaM kuNDU ]%pnna krta hO [sao vaatvaist khto hO maU~aosaMga maU~oind`ya Aqaa-t maoZ/ ko iCd` kI ivagauNata sao Aqavaa vaataxaop ko karNa qaaoDa saa maU~ ilaMga ko Aga`Baaga kI saMiQa maoM $k jaata hO. vah $ka huAa maU~ baad maoM pIDa ko saaqa yaa ibanaa pIDa ko saaqa yaa ibanaa pIDa ko inaklata hO.[sa $ko hue maU~ ko karNa raogaI kao maU~oind`ya maoM gau$ta ka AnauBava haota hO. maU~ jazr maU~ ko vaoga kao raoknao sao $ka huAa tqaa p`kuipt vaayau dvaara ]davai-tt maU~ AQaaomauK sao na inaklakr }pr baist maoM hI $ka rhta hO baist maU~ maoM Barkr jazrvat hao jaata hO.Aqaa-t ]dr p`doSa maU~ sao pirpUNa- baist sao Bara p`tIt haota hO.saaqa saaqa vaodnaa maU~avaraoQa purIYaavaraoQa tqaa Apak kI isqait haotI hO.
- 13. maU~atIt maU~ ko vaoga kao AiQak samaya tk QaarNa ike vyai> maoM maU~ svayaM SaIGa`ta sao p`vaRt nahIM haota.eosaa raogaI jaba maU~ %yaaganao baOzta hO tao maU~ mand vaoga sao Aata hO.mand gait sao baar baar maU~ kI p`vaRi%t kao maU~atIt khto hOM. vaistkuNDla yah BaI maU~atIt ko samaana hI jaOsaI isqait hO.Aacaaya- vaagBaT tqaa Aacaaya- sauEaut nao maU~atIt tqaa vaistkuNDla kao ek hI maanaa hO. Aacaaya- cark matanausaar [samaoM baist Apnao saamaanya sqaana sao }pr ]zI hu[- baZI tqaa gaBa- ko samaana p`tIt haotI hO.SaUla spMdna tqaa dah sao pIiDt raogaI kao baUMd baUMd krko maU~ Aata hO ikntu yaid vaist p`doSa kao haqa sao dbaanao pr maU~ kI Qaara inakla pDtI hO. AYzIlaa purIYa maaga- evaM baist ko baIca maoM AaiEat vaayau AYzIlaa ko samaana Gana Aqaa- t kzaor ga`inqa kao ]%pnna krtI hO yah ga`inqa isqar yaa [-Yat cala AaOr hu[- haotI hO.[sakao vaataYzIlaa khto hOM. maU~ga`inqa baist ko BaItr gaaola isqar CaoTI ga`inqa sahsaa Aa jaatI hO ijasamaoM ASmarI ko samaana vaodnaa haota hO.[sao maU~ga`inqa khto hOM.
- 14. ]YNavaat AiQak vyaayaama pdyaa~a tqaa Aatp saovana sao vaayau saiht p`kuipt huAa ip%t baist maoM isqat haokr baist maoZ/ tqaa gauda maoM p`dah ]%pnna krta hO AaOr hird`a ko vaNa- vaalaa r> imaiEat maU~ yaa kovala r> ka hI s~ava krata hO.[samaoM kRcC/ta ko saaqa baar baar maU~ ka s~ava haota hO. maU~Sauk` maU~ vaoga ko rhto s~I p`saMga krnao vaalao vyai> ka vaayau p`kuipt jaata hO.eosaI isqait mao Apnao sqaana sao cyaut huAa SaUk` maU~ %yaaga ko phlao yaa pScaat p`vaRt haota hO.eosao raogaI maoM maU~ Basmaaodk Aqaa-t caUnao ko panaI ko samaana safod tlaCt yau> haota hO.maU~ maoM Sauk` kI ]pisqait ko karNa kBaI kBaI maU~ maoM kRcC/ta tqaa maU~ivavanQa%va Aa jaata hO. ivaDivaGaat jaba purIYa vaayau dvaara ]davaRt haokr maU~maaga- maoM phuMca jaata hO AaOr malayau> yaa mala BaI ganQa sao yau> maU~ vaodnaa ko saaqa Aata hO. maU~saad ip%t AaOr kf Alaga Alaga Aqavaa ek saaqa p`kuipt vaayau dvaara GanaIBaUt hao jaato hOM tao raogaI kRcC/ta ko saaqa pIt r> yaa Svaot gaaZa dahyau> gaaoraocanaa tqaa SaMKBasma ko vaNa- ka Alp jala yau> tqaa tInaaoM daoYaaoM ko vaNaao-M sao yau> maU~ %yaaga krta hO. maU~xaya vaat dvaara maU~ ko saUKnao pr yaa Alp haonao pr maU~xaya haota hO.[samaoM vaat ko lxaNa haoto hOM.
- 16. URINARY TRACT INFECTION A urinary tract infection (UTI) is an infection of any part of the urinary system. Most infections involve the lower urinary tract. UTIs are given different names depending on where they occur: • Bladder infection - cystitis • Urethra infection - urethritis • Kidney infection - pyelonephritis The ureters are very rarely the site of infection. Most UTIs are not serious, but some can lead to serious problems, particularly with upper urinary tract infections. Recurrent or long-lasting kidney infections (chronic) can cause permanent damage, and some sudden kidney infections (acute) can be life-threatening, particularly if septicemia (bacteria entering the bloodstream) occurs.
- 17. INCIDENCE The incidence of UTI is more in females than males.Women are more likely to develop UTIs than men, due to anatomical differences; the urethra is shorter in women than in men, and it is closer to the anus, making it more likely that bacteria are transferred to the bladder. Over 50 percent of all women will experience at least one UTI during their lifetime, with 20-30 percent experiencing recurrent UTIs.
- 18. 67% 22% 7% 2% 1% 1% UTI causing organisms E.coli Klesiella Staphylococcus Psuedomonas Enterococcus Other gram -ve bacteria
- 19. RISK FACTORS The following factors can increase the likelihood of developing a UTI - Sexual intercourse (especially if more frequent, intense, and with multiple or new partners) Diabetes Poor personal hygiene Problems emptying the bladder completely Having a urinary catheter Bowel incontinence Blocked flow of urine Kidney stones Some forms of contraception Pregnancy Menopause Procedures involving the urinary tract Suppressed immune system Immobility for a long period Use of spermicides and tampons Heavy use of antibiotics (which can disrupt the natural flora of the bowel and urinary tract)
- 20. PATHOGENESIS The urine is normally sterile. An infection occurs when bacteria get into the urine and begins to grow. The infection usually starts at the opening of the urethra (where the urine leaves the body) and moves upward into the urinary tract. The culprit in at least 90% of uncomplicated infections is a type of bacteria called Escherichia coli better known as E. coli. These bacteria normally live in the bowel (colon) and around the anus. These bacteria can move from the area around the anus to the opening of the urethra. The two most common causes of this are improper wiping and sexual intercourse. Usually, the act of emptying the bladder (urinating) flushes the bacteria out of the urethra. If there are too many bacteria, urinating may not stop their spread. The bacteria can travel up the urethra to the bladder, where they can grow and cause an infection. The infection can spread further as the bacteria move up from the bladder via the ureters. If they reach the kidney, they can cause a kidney infection(pyelonephritis), which can become a very serious condition if not treated promptly.
- 21. SIGNS AND SYMPTOMS General Signs and Symptoms : Burning sensation while urinating Pain or Pressure in lower abdomen Cloudy , Bloody , Strange smelling urine Fatigue Clinical Signs and Symptoms : Lower urinary tract infection Bladder (cystitis): The lining of the urethra and bladder becomes inflamed and irritated. Dysuria: pain or burning during urination Frequency: more frequent urination (or waking up at night to urinate, sometimes referred to as nocturia); often with only a small amount of urine Urinary urgency: the sensation of having to urinate urgently Cloudy, bad-smelling, or bloody urine Lower abdominal pain or pelvic pressure or pain Mild fever (less than 101 F), chills, and "just not feeling well" (malaise) Urethra (urethritis): Burning with urination
- 22. Upper urinary tract infection (pyelonephritis) Symptoms develop rapidly and may or may not include the symptoms for a lower urinary tract infection. Fairly high fever (higher than 101 F) Shaking chills Nausea Vomiting Flank pain: pain in the back or side, usually on only one side at about waist level Symptoms with respect to age= Newborns- fever or hypothermia (low temperature), poor feeding, jaundice Infants- vomiting, diarrhea, fever, poor feeding, not thriving Children- irritability, eating poorly, unexplained fever that doesn't go away, loss of bowel control, loose bowels, change in urination pattern Elderly people- fever or hypothermia, poor appetite, lethargy, change in mental status
- 23. DIAGNOSIS Diagnosis will usually be made after proper history taking and testing a urine sample . A "clean catch mid flow urine sample " is used, which is where a person washes their genital area before collecting a urine sample mid-flow. This helps to prevent bacteria from around the genital area getting caught in the sample. The single most important lab test is urinalysis and urine culture test. A urine sample will be tested for signs of infection, such as the presence of white blood cells and bacteria. If a person has recurrent UTIs, a doctor may request further diagnostic testing to determine if anatomical issues or functional issues are to blame. Such tests may include: Urodynamics - a procedure that determines how well the urinary tract is storing and releasing urine Cystoscopy - looking inside the bladder and urethra with a camera lens inserted via the urethra through a long thin tube
- 24. Imaging tests are most often needed for the following groups: • Children with repeat urinary tract infections, especially boys.Up to 50% of infants and 30% of older children with a urinary tract infection have an anatomic abnormality. The child's pediatrician should investigate this possibility. • Adults with frequent or recurrent urinary tract infections. Blood tests usually are not required unless a complicated condition, such as pyelonephritis or kidney failure, is suspected.
- 25. NEPHROPATHY
- 26. NEPHROPATHIES Nephropathy is a broad medical term used to denote disease or damage of the kidneys, which can eventually result in kidney failure. The primary and most obvious functions of the kidney are to excrete any waste products and to regulate the water and acid-base balance of the body – therefore loss of kidney function is a potentially fatal condition.
- 27. TYPES The list of types of Nephropathy mentioned in various sources includes: • Toxin nephropathy - due to toxins damaging the kidneys • Obstructive nephropathy • Diabetic Nephropathy - due to diabetic hyperglycemia damaging kidneys • Reflux nephropathy • IgA nephropathy • Analgesic nephropathy
- 28. OBSTRUCTIVE NEPHROPATHY Obstructive nephropathy, also know as uropathy, refers to the syndrome caused by urinary tract obstruction, either functional or anatomic. It includes urinary tract dilatation, impedance and the resulting slowing of urine flow, change in the pressure inside the kidney tubular system and impaired kidney function. Blockage to the flow of urine leads to hydronephrosis and hydroureter. Obstructive nephropathy is a common condition, and its incidence rises with advancing age. In children, the leading cause is ureteropelvic junction obstruction, with an incidence of one in 1500. Urolithiasis in children occurs in 1-5%
- 29. 1. CAUSES:- Obstructive nephropathy may manifest in varying ways, from asymptomatic to acute renal failure. It may be acute or chronic, unilateral or bilateral. Acute obstruction is most often due to ureteral stones. Chronic causes range include: • Benign prostatic hyperplasia • Neurogenic bladder • urinary tract stones • ureteral stricture • congenital anomalies such as uretero-pelvic junction stenosis • Fibrosis of the retroperitoneum • Tumors of the ureter • Ureteroceles • Cancers of the colon or of the pelvic viscera • Metastatic tumors in the abdomen
- 30. 2. SIGNS & SYMPTOMS:- The symptoms of obstructive nephropathy may stem from the cause of obstruction as well as the dilated organ itself. Thus they include: • Back and loin pain, or groin pain • Fever • Nausea and vomiting • oliguria • Edema • Urgency or frequency of urination • Incomplete urination • Dribbling of urine • Hematuria
- 31. 3. PATHOGENESIS:- Because of any anatomical or functional dysfunction regardless of the specific cause, can cause back pressure on the kidney by preventing urinary flow. This can result in decreased renal blood flow, decreased glomerular filtration rate, and up- regulation of the renin-angiotensin system. This can in turn cause atrophy and apoptosis of the renal tubules and interstitial fibrosis with infiltration of the interstitial spaces by macrophages. These changes may lead to decreased re-absorption of solutes and water, inability to concentrate the urine, and impaired excretion of hydrogen and potassium. If left untreated, obstructive nephropathy can cause irreversible renal damage. Obstruction can ultimately cause tubulointerstitial fibrosis, tubular atrophy, and interstitial inflammation.
- 32. 4. DIAGNOSIS:- • Diagnosis is based upon clinical examination followed by imaging tests such as intravenous urography, retrograde ureterography, ultrasound, CT scans, and contrast imaging. • Ultrasound has become the imaging technique of choice because it is available almost everywhere and is safe but sensitive. • CT scans are especially useful in identifying retroperitoneal or pelvic growths which are obstructing the ureter. • Dye excretion urography will show the characteristic dense nephrogram in case of ureteric obstruction. • Renal scintigraphy using I123-hippuran or technetium scans are helpful in assessing kidney function in a less invasive way, including the accumulation of the isotope, its transit time and excretion. • There are several other methods such as perfusion pressure studies and renal scintigraphy to help differentiate obstructed urinary tracts from those which are only dilated. • Early diagnosis of urinary obstruction is vital to prevent further damage or to reverse renal impairment.
- 33. DIABETIC NEPHROPATHY Diabetic nephropathy (or diabetic kidney disease) is a progressive kidney disease caused by damage to the capillaries in the kidneys' glomeruli It is characterized by nephrotic syndrome and diffuse scarring of the glomerulli is due to longstanding diabetes mellitus Diabetic nephropathy is damage to your kidneys caused by diabetes. In severe cases it can lead to kidney failure. But not everyone with diabetes has kidney damage.
- 34. SIGNS & SYMPTOMS During its early course, diabetic nephropathy often has no symptoms. Symptoms can take 5 to 10 years to appear after the kidney damage begins. These late symptoms include:- • severe tiredness • headaches • a general feeling of illness • nausea • Vomiting • frequent voiding • lack of appetite • itchy skin • leg swelling
- 35. PATHOGENESIS Diabetes causes a number of changes to the body's metabolism and blood circulation, which likely combine to produce excess reactive oxygen species (chemically reactive molecules containing oxygen). These changes damage the kidney's glomeruli (networks of tiny blood vessels), which leads to the hallmark feature of albumin in the urine (called albuminuria).As diabetic nephropathy progresses, a structure in the glomeruli known as the glomerular filtration barrier (GFB) is increasingly damaged.This barrier is composed of three layers including the fenestrated endothelium, the glomerular basement membrane, and the epithelial podocytes. The GFB is responsible for the highly selective filtration of blood entering the kidney's glomeruli and normally only allows the passage of water, small molecules, and very small proteins (albumin does not pass through the intact GFB). Damage to the glomerular basement membrane allows proteins in the blood to leak through, leading to accumulation in Bowman's space .
- 36. DIAGNOSIS Diagnosis is usually based on the measurement of high levels of albumin in the urine or evidence of reduced kidney function. Albumin measurements are defined as follows: • Normal albuminuria: urinary albumin excretion <30 mg/24h; • Microalbuminuria: urinary albumin excretion in the range of 30–299 mg/24h; • Clinical (overt) albuminuria: urinary albumin excretion ≥300 mg/24h. People with diabetes are recommended to have their albumin levels checked annually, beginning immediately after diagnosis for type 2 diabetics, and five years after diagnosis for type 1 diabetics. To test kidney function, the person's estimated glomerular filtration rate (eGFR) is measured from a blood sample. Normal eGFR ranges from 90 to 120 ml/min/1.73 m2.
- 37. IgA NEPHROPATHY • IgA nephropathy (IgAN), also known as IgA nephritis, Berger disease or synpharyngitic glomerulonephritis, is a disease of the kidney (or nephropathy), specifically it is a form of glomerulonephritisor an inflammation of the glomeruli of the kidney. • IgA nephropathy is the most common glomerulonephritis worldwide. Primary IgA nephropathy is characterized by deposition of the IgA antibody in the glomerulus. There are other diseases associated with glomerular IgA deposits, the most common being IgA vasculitis (formerly known as Henoch–Schönlein purpura [HSP]), which is considered by many to be a systemic form of IgA nephropathy. • HSP presents with a characteristic purpuric skin rash, arthritis, and abdominal pain and occurs more commonly in young adults (16–35 years old). HSP is associated with a more benign prognosis than IgA nephropathy. • In IgA nephropathy there is a slow progression to chronic kidney failure in 25–30% of cases during a period of 20 years.
- 38. SIGNS & SYMPTOMS Signs and symptoms of IgA nephropathy when kidney function is impaired include: • Cola- or tea-colored urine (caused by red blood cells in the urine) • Repeated episodes of cola- or tea- colored urine, sometimes even visible blood in your urine, usually during or after an upper respiratory or other type of infection • Pain in the side(s) of your back below your ribs (flank) • Swelling (edema) in your hands and feet • High blood pressure
- 39. PATHOGENESIS IgA nephropathy appears to result from an ordered sequence of events, starting with galactose-deficient IgA1, which contains less than a full complement of galactose residues on the O-glycans in the hinge region of the heavy chains.. These may act as auto-antigens that trigger the production of glycan-specific autoantibodies and the formation of circulating immune complexes that are deposited in renal mesangium. These then induce glomerular injury through pro-inflammatory cytokine release, chemokine secretion, and the resultant migration of macrophages into the kidney.
- 40. DIAGNOSIS For an adult patient with isolated hematuria, tests such as ultrasound of the kidney and cystoscopy are usually done first to pinpoint the source of the bleeding. These tests would rule out kidney stones and bladder cancer, two other common urological causes of hematuria. A kidney biopsy is necessary to confirm the diagnosis. The biopsy specimen shows proliferation of the mesangium, with IgA deposits on immunofluorescence and electron microscopy. However, patients with isolated microscopic hematuria (i.e. without associated proteinuria and with normal kidney function) are not usually biopsied since this is associated with an excellent prognosis. A urinalysis will show red blood cells, usually as red cell urinary casts. Other renal causes of isolated hematuria include thin basement membrane disease and Alport syndrome, the latter being a hereditary disease associated with hearing impairment and eye problems. Other blood tests done to aid in the diagnosis include CRP or ESR, complement levels, ANA, and LDH. Protein electrophoresis and immunoglobulin levels can show increased IgA in 50% of all patients.