Nephrology PDF - Glomerular Disorders

NEPHROLOGY GLOMERULAR DISORDERS Are group of glomeru lar inflammatory disorders resu lt ing mainly from an immun ologic in su lts Immunological injuries Immune complex reaction It is an antigen- anti body comp...

NEPHROLOGY GLOMERULAR DISORDERS Are group of glomeru lar inflammatory disorders resu lt ing mainly from an immun ologic in su lts Immunological injuries Immune complex reaction It is an antigen- anti body comp lex result ing as a react ion of ant ibodi es against exogenous antige11 The complex precipitate in glomeru li and init iate immunologic Nephron infl ammatory changes It represent a 95% of cases Autoimmune reaction Antibod ies are formed against body own t issue i. e. it is a reaction against endogenous antigen Antibod ies precipitate in g lomeru lar basement membrane and initiate immu no logic inflammatory changes Glomeruli Pathological Aspect The infl ammation resu lt ing from immuno logic reaction may be in form of Proliferative glomeru lar inephrit is Memberanous glomeru lonephritis Membranoproliverstive GN Foca i giomerui ar sde rosis Diffuse mesinegeal proliferat ion Clinical Aspects The clinical syndromes resulting from ,patho logica l and im munologic changes are: Nephrotic syndrome Nephritic syn drome Nephrotic-nephritic synclrome 240  N E p H R O L O G V NEPHROTIC SYNDROME It is a clinical syndrome charatteirized by: M assive proteinuria : more than 50 mg/kg/ 24h in child re n or urinary protein/creatinine ratio>2 Hypoproteinemia : serum albumin -J,, 2.5 gm/di. Hyperlipideamia : serum cho lestero l 1' 250 mg/di. Ge neralized ede ma. Heavy proteinuria is the hall mark of nephrotic syndrome CAUSES I ,----------- ----------- --- ---------------, I I I Primary Secondary Kidney is the maim invoh,ed organ : Occur during a course of system ic Dis. Common infections :bilharzia hepatitis B malaria. Minimal lesion NS (most common ) Diffuse mesangial proliferation Collagen : systemic lu pus. Foca l glomeru losclerosis Blood : sickle ce ll An. Uncommon Tumour: lym phoma, lel!kemia. Metabolic : diabetes Membranous glomeru lonephriti,s Drugs : gold, mercury Membranoproliferative GN. Congenital nephrosis Minimql Change Nephrotic Syndrome - It is t he most common ca use of nephrotic synd. in ch ildren. fJC ' I I It accou nts about 90% ·o f causes of nephrotic synd. [/., Etiology ~ D~ Podocyte With Normal Foot Process It is not well kn own, but it is proposed that it is a result of Teel I dysfunction by t wh ich T.ce lls secretes lymphokines ➔ glomeru lar permeability to protein s ➔ protein loss in urin e. Pathology By light microscope: No abnorma lit ies could be detected. By electron microscope: on ly fus ion of foot processes of epithelial ce ll s Min ima l change NS that invest t he glomerular capill aries (podocytes). (fusion of foot processes) 241  N E p H R O L O G V Pathogenesis Proteinuria: is due to 1' glomerl!Jlar permeability to proteins ➔ protein loss in urine. Prote inuria is selective i.e lloss of low molecular weight proteins [mainly albumin]. Hypoproteineamia : Due to loss of proteins in urine. Hyperlipidaemia : is due to : Hypoproteineamia stimulate the liver to produce lipoprote in ➔ 1' lipid production. Loss of lipase enzyme in urine ➔ -J,, destruction of lipids. Edema : is due to : Hypoproteineamia ➔ -J,, pl asma prote in s ➔ -J,, osmotic pressure ➔ t ra nsmission of fluids from intravascular to interstitial tissue ➔ edema. Hypovolemia ➔ 1' antidiure.tic h~rmone ➔ water retention. Hypovolemia ➔ rena l ischemia ➔ stimulation of ren in-angiotens in system ➔ stimulation of aldosterone secretion ➔ Na and water retention. T cell (abnormal lymphokiens) 1'glo1111erular premability to proteins Loss of immunoglobin Hypoalbuminemia & properdin factor -J,,osmotic pressure of plasma + protein ➔ transm ission of fluid Edema ~ ◄----------­ from intravascu lar to interstial compartment + Corticosteroid therapy Hypovolemia hemoconcentration & Infection Hypotension, shock, renal fa ilure , thromposis 242  N E p H R O L O G V Clinical picture Generalized edema: Is the presenting symptom, it starts as periorbita l edema and extend to invo lve lower limbs with sacral edema, scrotal edema and anterior abdomina l wall edema. Ascites: In severe cases, the edema is associated with ascites. Priorbital edema Respiratory distress: May be due to, severe abd. distension, associated pleural effus ion or associated chest infection. Subcutaneous pitti ng edema GIT manifestation : Anorexia, abdom ina l pain and diarrhea due to intestinal edema. Complications Hypovolemia : Hyptotens i on ➔ Hypo-volemic shock ➔ Pre-rena l fa ilu re. Infections-due to: - Loss of lgs in urine. - Loss of properdilil factor (comp lement factor )in urine. - Edema is a gbod media for infection. - Corticostern id therapy. - Hypoperfusion of spleen (splen ic hypofunction). - Most common infections are o Urinary tract infection o Pneumococcal peritonitis o Pneumonia o Cellulit is o Septicem ia o Most common organisms: pneumococci, men ingococci & H. Scrotal edema inf leuenza. Thrombosis is due to : - Hemoconcentrati0n. - Hyperli pid aemia. - 1' plate let aggregation. - Loss of ant it hrombin e Ill in urine - Thrombosis common sit es are: o Rena l vein thrombos i s ➔ hematuria & abdom ina l mass. o Pu lmonary thrombos i s ➔ severe chest pain. o Mesenteric thrombosis ➔ acute abdomen. o Cerebra l thrombos is ➔ vascular hemiplegia. Malnutrition and growth retardation. 243.,,............. N E p H R O L O G Y Investigations Urine Routine urine analysis proteinuria +++ hematuria may be microscopic in 25% of cases Casts: hyaline & gran,ular cast because urinary protein precipitate in t he tubu les Protein in 24h. urine : 1' 50 mg/kg/24h. Protein/creatinine ratio: 1' 2. It is an easy, rapid method, needs no collection of 24 h urine (used in infancy, the normal range is 0.2-0.5) Urine culture: for evidence of urinary tract infections. Blood -i pla sma protein. -i 5.5 gm/di [normal 6.5 -7gm/dl]. -i serum albumin -i 2.5 grin/di [normal 3.5 gm/di]. 1' serum cho lesterol 1' 250 mg/di Urea and creatinine are usually normal. Other CBC :increased hematocrit C3 is normal Hepatitis B&C markers Renal biopsy I ' MLNS is characterized by: Renal biopsy is indicated Age of onset 1-10 yr Age below 1 y. or above 12 ys. No macroscopic hematuria. macroscopic hematuria No hypertension Persistent hypertension. Good respond to Corticosteroid resistant. corticosteroid. Renal dysfunction Normal renal function Low C3 Normal C3 Treatment Non specific treatment Sa lt restriction and high protein diet. IV salt free albumin [0. 5-lgm/kg] over 2hours, fo llowed by IV Lasix lmg/kg it can be repeated every 12 hours under monitoring of blood pressure. 244  N E p H R O L O G Y Diur,etics: one or two of the fo llowing - Lasix 1-2 mg/kg ora l - Spironolactone' 2-3 mg/ kg - Chorothiaz ide ~10 mg/ kg/dose every 12 hours) Metilazone (th'iazide li.ke 0.1 mg/ kg / dose ora ll ). NB Use of massive diuretics is risky as they can lead to more hyporvo lem ia ➔ decrease rena l blood flow wh ich leads to acute tubu lar necrosis.. Specific treatment By predn isone 2mg/ kg/ day ora lly divided into 3 doses (maximum 60mg per day) for 6 weeks. After 6 wee ks, exam ine urine for prote inuria for 3 days I 1------ ----------------- --- -, I I , __ _ __.__Y_ _ _ ___, Still proteinurea No proteinurea Corticosterq id res istant (Corticostero id responder) I I y Start mainta ince therapy Rena l biopsy Maint an.ce therapy It is an alternat ive day therapy: (one dose early morn ing, after Breakfast) By Prednisone ➔ 1.5 mg/ kg / every other day for 1-2 months. 1mg/kg /every other day for the 1-2 months. 0.5 mg/kg/ every other day for other 1-2 months. Treatment of Relapse st. - -- ~ -- - - ~ After 1 attack of nephrotic synd., 4 possibilit ies can occur: Cyclophosphamide & No recurrence: (None re lapsing): ➔ Requ ires no treatment. st cyclosporeins are most Infrequent relapse : (2-3 re lapses/ year) ➔ treatment as 1 attack. commonly used Freq uent relapse : (4 or more relapses/ year). cyt otoxic drugs Corticosteroid dependent : Rel apse 2 weeks after stoppage of corticostero id or during drug withdrawal Indication of cytotoxi'c drugs in nephrotic syndrome. Corticosteroid resistant (no response after 6 weeks of steroid th erapy) Frequent relapses. Corticosteroid dependent 245  N E p H R O L O G V PROTEINURIA Presence of protein in urin e more than 150 mg/24 urine in adult. presence of protein in 1urin e more than 4 mg/kg/ 24 h in chi ldre n Proteinu r ia is classified into :: - Nephrotic range prote inuria > SOmg/kg/d - Non nephrotic rang,e more than 4 mg/kg/d and less t han 50 mg/kg/d Detection Qualitative Urine dipstick principally ,detect the albumin Normal : negative Trace (10-20 mg/di), 1+ (30 mg/di), 2+ (100mg/dl), 3+ ( 300mg/dl), 4+ (1000-2000mg/dl) Quantitative Urinary protein/ creatnime ratio: normal ( 0.2 -0.5). 24 hours co llection of unine Causes Non pathologic Severe exercise. ~ Postura l prote inuria [1' i!n protein !oss in upright position ] Febrile illness..-l ln_v_e-st- ig - a-.t-io_n_s_a_r_ e _n_o_t -n-ec_e_s-sa- r-, ~ Pathologic Tubular: due to defect of abs0rption of normally filtered proteins as in : 1. Fanconi syndrome 5. Cystinosis. 2. Ga lactosem ia 6. Vit. D intoxicat ion. 3. Wilson dis. 7. Renal tubu lar acidosis. 4. Lowe's syndrome. 8. Interstit ial nephritis. Glomerular: Nephrotic syndrome : causes of nephrotic syndrorne - Glom eru lar nephritis : causes of GN Others: UTI , drugs , tumors (l;ymphoma), stones 246  E p H R O L O G V NEPHRITIC SYNDROME It is a clinical syndrome characterized by Hematuria with RBCS oast RBCS casturia is the Oliguria hallmark of nephritic Hypertension syndrome Mild generalized edema Hematuria means more t han 5 RBCS /lOCC fresh voided urine sediment by high power fie ld Causes of nephritic syndrome Poststreptococca.l GN. lgA nephropat hy. Alpert syndrom e. M ernbranopro liferative (M PG N). System ic lupus. Heonch scholi en GN. Good pasture syndrome. Post streptococcal GN is the most common cause of nephritic syndrome in children ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS (APSGN) It is the most common type of nephritis in crni ldhood. Etiology It is non suppurative comp lication of group A ~ hemolytic streptococci [n ephrogen ic str,ain], serotype [12 (pharyngit is )-49 (pyoderma )]. APSGN: Occurs common ly after skin infection (impetigo] and scarlet fever and less common ly occurs after pharyngitis. Pathogenesis It is an immune complex disease " by which the body forms antibod ies aga inst streptoccoa l ant i gen ➔ antigen antibody comp lex [ca ll ed immune complex]. The 1 complex circu lates in blood into the glomeru li where it stimulates the inflamm atory reaction w,ith deposition of the complement. 247  N E p H R O L O G V Streptococca l infection I ,, I [Most common skin and scarlet fever] Less common pharyngitis, after 2- 3wks latent period] I I I Immun e comp'lex is formed in patient's serum, circul ate into glommeruli ➔ deposit ion of immune complex and complement in glomeruli lnflammatt ry changes with proliferation and necrosis of glomeru lar ce lls. _____________ l ____________ _ I I + Narrowing of capillary Hematuria lum en ➔ ,_J,, glomeru lar filtrat ion rate r---- -- ---------- - --- Olig~ ia Hyper volemia ,, I ,,I In severe cases Edema & hypert ension Anuria - Hypertensive Rena l fa ilure encephalopathy and or heart failure Pathology The pathological lesion is characterized by : Proliferation of ep ithelia,I and endothel ial glomerular cells. Ce llular infiltration. Edema and t hickening of the basement membra ne. Narrowed capillary lumen. 248  N E p H R O L O G Y Clinical picture 1Gross hetnaturia Age incidence 2- 6 years History of skin infection, scarlet fever or pharyngit is 2-3 w ks age. Dark urine wit h dim inished urinary out-put are the most freq uent mam ifestat ion. In first days, t he urin e is grossly blood, and t hen becomes smo ky. Edema: o Is usua lly mild (puffy eyes+ edema low er li mbs). o It may be massive if cond it ion i s associated with : Heart fa ilu re. Rena l fa il ure. Smoky u r ine Nephros is [n ephrit ic - nephrotic syndrome]. Hypertension : M ild to moderate hypertension is usua l Oliguria: o In infa nts is (less t han 1 m l/kg/h) o In chil dhood (less tha n S00m l/day Complications Heart failure : Respiratory, distress w ith wh eezy chest. Pu l. Edema w it h basa l crepitation may occur. Card iomega ly and tachycard ia. Congested neck ve ins and congested tender liver. Renal failure Anuria - Acidotic breathing Ca rdiac arrhythmia. Coma and convulsions. Hypertensive encephalopathy : It is due to severe hypertension ➔ headache, vom iting, dizziness blurred vi sion even loss of vision genera lized convu lsion Investigations Urine : routine urine analysis for : Hematuria : is a co111stant feature. RBCs casturia : RBCs bind ing with tubu lar mucoprotein. Proteinuria : mild 1+ or 2+ by dipstick. 249  N E p H R O L O G Y Pyuria : may be prese nt. N.B Blood for: evidence of streptococcal infection Nephritis with -1, (3 1' ASOT, if not 1' ask for anti-Ant i-DNAse B & antihyaluronidase or occur in : Streptozyme are alternative tests. ASOT is increased when nephritis PSGN fo ll ows streptococca l pharyngitis , it is normal if nephrit is fo llows skim Systemic lupus. infection as streptolysine O is bound to skin li pid, so normal ASOT does not ru le out the diagnos is of PSGN MPGN Serum complement [C 3 ] is~- Infective Renal function urea, creatinine & serum electrolytes. endocarditis Differential Diagnosis Between Nephritis And Nephrosis: Item Nephritis Nephrotic History of strep. +ve -ve Hematuria. +ve -ve Blood pressure. hypertension hypotension Oedema mild massive Ascites.J ve may be present Proteinuria Mild -1,50mg/kg/ 24h. Massive 1'50mg/kg/ 24h. N.B. If the manifestation of nephrotic syndrome and nephritis are present in t he same patient e.g. [hematuria w it h massive proteineuria] the condition is ca lled [nephritic nephrotic syndrome] and rena l biopsy is indicated. Prognosis Macroscopic hemat uria disappears w ith in 4 we eks Microscopic hematuria can persist for one year Sponta neou s resoiut ion in more than 95% of cases 5% may develop chronic GN Recurrence is extremely rare Prophyl actic long acting pen ici llin is not in dicated. Treatment Hospitalization. Treatment of streptococcal infection [if there is evidence of strep·. infection ]. by: pen i~i llin ➔ 10 days or erythromycin in pernicill in sensitivii y Fluid chart : 2 Fluid inta ke / 24 h = Uri ne output+ insensible water loss [400cc/ m surface area] in chi ld ren.Or (30m l/kg/d )for infants. 25Cl  N E p H R O L O G V Treatment mild to moderate Hypertension (one or more of followings) Lasix 1!-2 mg/kg/d Ca Channel blocker (n eifidipine 0.Smg/kg/d ) captopril 01.2'-2mg/kg/d Treatme nt Severe hypertension with heart fa il ure or encephalopathy o Niffed ipine sublingeal 0. Smg/kg/dose repeated as needed after 30 -60 min + iv diuretics o In re:s istant cases: nitroproside ( vasodila,t or), labeta lol IV (a & B blockers) can be used. Treatment of rena l fa il ure: [see ttt of acute renal failure]. Causes of Hypertension ~----~-----------------------, ' --~S=e=c~o=n-d-ar_v_ _ Essential , -----------------~ I Non renal I I En.docrinal I unknown cause I hyperthyroidism- but it can be hyper parathyroid ism Rena l caushing synd. (1' affected by : co rtison e). glomeru lonephritis pheochromocytoma (1' Obesity pylo'nephritis. catecholamine). tsalt intake renal tumour. Cardiovascular aortic stress coaractation. polycyst ic kidney. hereditary Metabolic: obstructive uropathy. hypernatraemia. fa ctor hypercalcaemia. Drugs : cortisone. CNS: int racrania l t ension Gu illiane Barre syndrome 251  · ' ~ - ·· N E p H R O L O G Y URINARY TRACT INFECTION, (UTI) Infection of urinary tract is classified according to site of infection Cystit is: infection of urinary bladder. Pyelonephritis : infection of t he kidn eys. UTI in children is important because Up to 60% of patient have structura l anoma lies of urinary tract. Pyel onephrit is leads to damage of growing kidn ey leads to renal scars , if bi lateral can leatll t o chronic renal fa ilure. Etiology Causative organisms : Gram - ve : Ecoli [m ost commo n], Kl ebsiell a, Proteus and Pse ud omonas. Gram +ve : e.g. Streptococci and Staph. Route of infection Ascending: Most common routt e of infect ion by which the organism ascends t hrough urethra to infect bladder and kidn eys. Ecoli is usually the invad ing organ ism and vesico ureteric reflex is usually t he predisposing factor. Hematogenous : Less commol'il, it occurs secondary to chest infect ion, osteomyelit is, septi,cem i.a. Predisposing factoris = [causes of recurrence] o Functiona l abnorma lit ies: immun odeficiency. vesico -ureteric reflux. o Anatomical ab n ormal i t i es ➔ obstruction e.g. - Pelviureteric obstruct ion. - Bladder diverticu lum. - Ureteric stricture - Cong.posterior urethral valve. - Renal stone. Age and Sex : o In neon atal period: UTII is equ ally distri bute d between both sex. o In infa nt ile period [1st 2yr] : it occurs 6 t imes more in fema le. o In childhood: it occurs 3 t im es more in female t han male. o The girls are more affected t han boys due to re latively short urethra of female and easy fecal contam in at ion of urethral orifi ce ➔ ascend ing infection. 252  N E p H R O L O G V Vesico-ureteri c reflux o It is t he most common anoma ly pred is'pos ing to UTI. o It is a reflu x of urine from bladder into ureter and re n.al pelvis. o It is five gnades. II Ill IV V - Grade (I} : refl ux into ureter on ly - Grade (II} : reflux into rena l pelvis - Grade (111} :as Grade.(II} in add it ion to uretric d,ilation - Grade (I V}: as Grade (I ll } in add ition to di lation of rena l ca lyces - Grade (V):markec!l blunting of ureters and rena l ca lyces Clinical picture Neonatal Infantile fever or hypotherm ia refusa l to feed Irritability poor suckling Fever of unknown cause vomiting Recurrent vomit ing and diarrhea. fai lure to ga in wt Failure to thrive jaundice Childhood: Cyst i tis ➔ dysuria, urgency, frequency & suprapubic pain Pyelonephritis ➔ fever ,rigor & abdomina l pa in. Investigations Urine analysis Pyuria turinary WB C Opus ce ll s) ➔ 1'5 WBC in 10 cc fresh urine it is suggestive not diagnostic because: Pyuria may present in febri le children w ithout UTI as in ch ildren with genital infection (ba lan itis or vulvovaginitis}. Pus in urine.I t may be absent inspite of UTI as they lyse during storage. Microscopie:: hematu ria is common & Proteinuria is less co mmon. 253  N E p H R O L O G Y Dipstick : positive leucocyte esterase& nitrite test. Urine culture: Sample collection children : midstre.am urine sample infancy & neonates o catheter sample Renal Image For o suprapubic aspiration Transfer the sample to culture media in less than one hour Recurrent cases Transport in an ice bag if it takes a longer time Atypica l UTI Positive urine culture result: UTI wit h septicemia For midstream sample Increased creatnine o 10,000 colony / ml urine of single organism is contaminated Abdominal mass samples Resistant to ttt o 10,000-100,000 colon;,,,/ ml urine ➔ suspicion (Repeated ) non Ecoli Infection o More than 100,0GlO colony/ ml is diagnostic. Catheter or suprapubic sample o Any growth of a singl e organism/ mml in is diagnostic Blood for ➔ urea, creatinine Renal image Abdominal ultrasound: screening for congenital anomalies. Micturating cystourethrogram (MCUG}: to diagnose Vesi co ureteric- reflux Dimercapto-succinic acid scan (DMSA}: for detection of renal scars Treatment By specific antibiotics accordirng to culture and sensitivity test for 7-10 days MUCG ➔ VUR The most common used drugs are Cotrimoxazole: trimethoprim 'Smg/kg/d + sulphamoxazole 2S mg/kg /d Amoxicillin SO mg/kg/day Na!idixi c acid 50 mg/kg/day Cep halosporin SO mg/kg/day In severe cases, parenteral {ampicillin and gentamycin) or ceftriaxone can be used for 3-4 days and then1oral antibiotic can be started DMSA ➔ RT.kidny scar Prevention of UTI High fluid intake. Girls should wipe themselves after micturition from front to back. Empty bladder comp lete ly & regwlarly. Avoid constipation. In case of vesico-ureteric reflux, prophylactic antibiotics therapy in form of cotrimoxazole in half dose used once da ily for 6- 12 months. 254  N E p H R O L O G Y ACUTE RENAL FAILURE Definition Acute reduct ion of renal functions with inabi lit y of the kidneys to maintain normal biochemical hom eostasis. It is characterized by: Water imbalance ➔ ol iguria Electrolyte im ba l ance ➔ J.. Na, tK, J..( a, tP. Acid- base im ba lance ➔ metaboli c acidosis. Retention of waste products ➔ t urea and creatinine. Causes Pre renal failure: Hypovolemia Loss of water (dehydration) Blood Flow Loss of bl'o0d (Hemorrhage) Loss of plasma (Burn). Loss of plasma p'rotein (nephrotic synd.) Hypotension Shock Septicemia Heart fai lure Hypoxia : asphyxia &pneumonia Renal Acute GN; post strept ococca l GN, lupus nephritis, membrane- proliferative GN. l ➔ prerena l ,,, Acute tubular necrosis: 2 ➔ rena l Persistent 0f prerena l cause. 3 ➔ post renal Drugs : gentamycin Causes of ARF Nephrotoxins Acute Vascu lar: e.g hemolytic ureamic syndrome : triat of Acute renal fai lure Hemolytic An. Thromocytopen ia. Post renal: (obst ruct ive uropathy): e.g bilateral rena l stones Bilatera l pelviu reteric obstruction. Posterior uretheral valve obstruction. 255...-- '..,-- ' ,,......,.._. -. , N E p H R O L O G V Pathogenesis A- Oliguria in prerena l fa ilure it is due to ,J., renal blood flow. in renal failure, it is due to ,J., glom eru lar infiltration in post renal, it is due to obstruction of urine outflow. Electolyte imbalance Hyponatraemia: in ren al failure, there is water and Na retent ion but hyponatraemia occurs du e to excess fluid intake ➔ dilutional hyponatraemia. Hyperkalaemia: due to: - K. retention - Release of K outside the ce ll due to catabolism. t - Metabolic acidosis w ith t H+ ➔ exchange bet ween H+ and K+ at ce llular membrane ➔ discharge of K in blood. Hypocalcaemia and hyperphosphatemia: It is due to phosphorus retention ➔ hyperphosphatemia with 2.ry hypocalcaemia. Acid-base imbalan5 RBCs RBCs casts Dysmorphic RBCs Yes NO Glomerular Hematuria Non Glomerular Hematuria Stepl Stepl CBC,Urea ,creatn ine , serum Urine cu lture electro lytes ,C3&C4 Step2 Step2 Rena l image to detect rena l ASOT for PSCGN anoma lies, cystic disorders or Step 3 stones. ANA ,ant i DNA for lupus, blood Step 3 cu lture for infective Ca lcium in 4 hours urine endocarditis Sick le cel l anemia screen Step4 Step4 Renal biopsy for undiagnosed Cystoscopy for undiagnosed cases cases Indications Of Renal Biopsy In Nephritic Syndromes Persistent Causes of dark urine hematuria>lmonth Hematuria (glom eru lar) ➔ co la colored or smoky Recurrent hematuria. urine Massive prote inuri a + Hematuria (non glomeru lar) ➔ bright red urine. hematuria. Hameoglobinuria (G6PD) ➔ brown ish or dark red. Renal dysfunction. Bilinubinuria (hepat itis) ➔ dark yell ow or orange Normal comp lement. colored. Drug induced (rifampicin) ➔ red ur ine. Food (beet roots ) ➔ red urin e. Urates ➔ red urine. 261