50year male with Diabetes,Renal failure ,Papular lesions with koebner Phenomenon

CHIEF COMPLAINTS

 50 year male farmer by occupation came with complaint of

Itching in the front and back and both upper arms(since 2 months)

Nausea,loss of appetite(since 7days)

Decreased urine output(since 1day)

HISTORY OF PRESENT ILLNESS

He started his career at the age of 13years(1986) as lorry cleaner who used to accompany with driver for the first 2years.At his 15years age started driving the lorry by himself.

Till 45years(2019) he continued the same profession.He used to drive 100km to and fro in a day.Depending on his requirement of money he used to work 4-6 days in a week.

5 years back as he was getting tired easily(not able to drive long distance)went to local hospital, diagnosed as having high sugars started on OHA.He stopped driving as it is more stressful and started farming his 3 acre land.

He used OHA for 1year,later swithed to insulin as sugars were not in control.From 4years he is on inadequate dose of insulin.He used to take insulin dose (16U/18U) once in a day(against to  twice a day dose prescribed by doctor) bcz whenever taking twice a day, intermittently he was having hypoglycaemic symptoms like sweating, palpitations,weakness.

2years back he had trauma(thorn prick) to left second toe, it got worsened after getting treatment for 15day by local rmp.Came to our hospital,disarticulation of left second toe was done.

From one year patient is having on and off pitting type of  pedal edema till knee.No history of any associated orthopnea/PND 

2months back he had itching at the back more at night.Itchy lesions gradually spread from back to front, buttocks,upper arms.

From 7days patient is having symptoms of nausea, loss of appetite.From 1day he was having decreased urine output, came to our hospital for further management.

No history any fever,orthopnea,PND,dyspnea

PAST HISTORY

k/c/o DM2 - 5years back(1year-used OHA,from 4years he was on insulin once daily)

No history of Hypertension,asthma,TB,epilepsy,thyroid disorders

In October 2022,patient had complaint of both lower limb and upper limb weakness(not able to get up from bed),he was diagnosed as hypokalemic paralysis(sr k -1.7meq/l),with potassium correction he regained his power in the lower limbs and upper limbs.He used syp potcklor for 1week.No similar episodes subsequently

PERSONAL HISTORY

He wakes up at 7:00am in the morning,go his his farm, water his field and comes back at 10:00am eats tiffin.At 11:00am he goes back to farm and till 6:00pm he works there.Take insulin in the afternoon before eating lunch.After coming home, he bathe and eat food at 8:00pm and sleep's by 9:00pm

He had two 2daughters.All are married and having children.

Addictions : he eats umber,drinks alcohol during occasions and family gatherings

FAMILY HISTORY

No similar complaints in the family

MEDICAL HISTORY

He takes inj insulin S/C once daily

GENERAL EXAMINATION

Patient is conscious, coherent,co-operative.Moderately built and Moderately nourished.

Blood pressure-140/80mmhg,right arm, supine position

Pulse-90/min,regular rythm,normal volume.

Respiratory rate-18/min,thoraco abdominal

Temperature-98 F

Spo2-98% on room air

Grbs-420mg/dl

No pallor, icterus,clubbing,cyanosis,lymphedenopathy,edema of legs

No raised JVP

SKIN examination :-

Papules present over back, front,upper arms, buttocks.Koebner phenomenon +.

Hyperpigmented patches diffusely present on back front and over upper arms.Right foot plantar keratosis present.

Left foot second toe is absent

SYSTEMIC EXAMINATION

CENTRAL NERVOUS SYSTEM :

Higher mental functions

-Patient is conscious, coherent,co-operative.Oriented to time, place,person.

-Speech = Fluency,comprehension,repetition intact

-Memory =Recent,Remote,Immediate : Intact

Cranial nerve examination -

2 - Visual acuity RE-6/60,LE-CF 1mts

other cranial nerves are normal

Motor examination :

Bulk of muscle normal on both sides on inspection

Hand grip 100% on both sides

Tone 

                          Right.             Left 

Upper limb.    Normal.           Normal

Lower limb.    Normal.           Normal

Reflexes

                   Right.              Left

Biceps.       -                       -

Triceps.      -                       -       

Supinator.  -                        -

Knee.          -                        -

Ankle.         -                        -

Plantar.       flexor                  flexor

Sensory examination:

1.Spinothalamic:      R              L

Crude touch            +                +

Pain                         +                +

2.Posterior column:

Fine touch                +                +

Vibration     Reduced

          ankle     - -                   --

          Knee.     --                   --

          Wrist.       6sec          6sec  

Position sense 

         LL.            Rt-6/10.          Lt --5/10   

3.Cortical

Stereognosis:     +             +

Graphesthesia    +.            +

CEREBELLUM:

Finger nose and finger finger test were normal

No dyadiadokokinesia 

No pendular knee jerk

Heel knee test : normal

CARDIOVASCULAR SYSTEM :

-Elliptical & bilaterally symmetrical chest

-No visible pulsations/engorged veins on the chest

-Apex beat seen in 5th intercostal space medial to mid clavicular line

-S1 S2 heard

-No murmurs

RESPIRATORY SYSTEM

  Upper respiratory tract normal

  Lower respiratory tract :

-Trachea is central

-Movements are equal on both sides

-On percussion resonant on all areas

-Bilateral air entry equal

-Normal vesicular breath sounds heard

-No added sounds

-Vocal resonance equal on both sides in all areas

PER ABDOMEN :

-Scaphoid

-No visible pulsations/engorged veins/sinuses

-Soft,non tender, no guarding and rigidity, no organomegaly

-Bowel sounds heard

PROVISIONAL DIAGNOSIS

Uremic symptoms(secondary to CKD)

Papular lesions on upper trunk, back,buttocks and upper arms with Koebner phenomenon 

?Diabetic neuropathy

With H/0 hypokalemic paralyses(in oct 2022)

k/c/o DM2(Since 5years) 

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INVESTIGATIONS

In oct 2022,when he had the episode of hypokalemic paralysis

In our hospital on 22-4-2023

FINAL DIAGNOSIS

AKI ON CKD(Initiated dialysis on 23-4-2023)

Papular lesions with koebner phenomenon(?Lichen planus ?Lichenoid drug eruption ?Uremic pruritis)

History of Hypokalemic paralysis in oct 2022(sr K+ =1.7meq/l)

Left foot second toe disarticulated in 2021(secondary to trauma-thorn prick)

?Diabetic Neuropathy

k/c/o DM2(since 5years)

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Indication of dialysis in this patient =Anuria with  Uremic symptoms(nausea, loss of appetite)

After dialysis(On 23-4-2023) patient symptoms improved

Post dialysis RFT

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Pathophysiology of Hyperglycemia and Renal Failure

Generation of reactive oxygen and nitrogen species (RONS) induced by hyperglycemia

Increased stimulation of glucose oxidation pathways in non-insulin-dependent cells leads to the activation of alternative pathways, increased production of RONS and oxidative stress (OS) in hyperglycemic state.

Glucose auto oxidation

In glycemic homeostasis and in the absence of oxygen, glycolysis is the primary energy source in the cells.

The synthesis of substrates by glycolysis activates two other energy pathways: the tricarboxylic acid cycle (or the Krebs cycle) and the electron transport chain (ETC) (or the oxidative phosphorylation) in the mitochondria through protein complexes

In DM, the hyperglycemic state promotes the overactivation of the three main energy pathways previously described. The increased stimulation of glycolysis and Krebs cycle result in elevated production of reduced flavin adenine dinucleotide (FADH2) and reduced nicotinamide adenine dinucleotide (NADH), fed into the ETC.

The ETC is a source of reactive oxygen species (ROS), especially in renal cells, which have a large number of mitochondria

Ros which are harmful to mitochondrial DNA causes mitochondrial dysfunction by inhibiting the mammalian target of rapamycin complex 1 (mTORC1) and the AMP-activated protein kinase (AMPK). These changes alter the activation of the peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and thereby affect mitochondrial biogenesis, by increasing mitochondrial fission and the synthesis of defective mitochondria

This can lead to impairment of the ECT functions, with reduced synthesis of ATP, leading to renal cell lesion and apoptosis

In addition, increased glycolysis causes hyperactivation of polyol and hexosamine metabolic pathways, and increases the synthesis of AGEs and activation of PKC. This also result in decreased ATP levels, contributing to mitochondrial dysfunction and fragmentation

Schematic representation of the pathways preceding glycolysis and induction of oxidative stress. ETC: electron transport chain; 1,3-BPG: bisphosphoglycerate; G6P: glucose 6-phosphate; G3P: glyceraldehyde-3-phosphate; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; F6P: fructose-6-phosphate; F-1,6-P: fructose-1,6-phosphate; PKC: protein kinase C; AGE; advanced glycation end-products