Mr H, a 45-year-old solicitor and father of three, visited his GP Dr P with a persistent headache. He described two months of symptoms, occurring up to six times per week, mainly in the mornings and with associated nausea. 

Dr P took a thorough history and neurological examination, including fundoscopy. He excluded alcohol, stress or carbon monoxide poisoning as potential precipitants, and found no other ‘red flag’ symptoms. Mr H mentioned that a close friend had been diagnosed with a brain tumour a few years ago. He was not particularly worried about this, but Dr P decided it should be excluded and referred him for an early neurological opinion. 

As part of his examination, Dr P checked the patient’s blood pressure and found it to be elevated at 164/89. A follow-up visit was arranged with the practice nurse a few days later and this had reduced to 132/72. No further action was taken. 

Mr H was seen by neurologist Dr B some six months after his initial GP presentation, and underwent an MRI scan. The scan was normal and Dr B advised Mr H that his headaches were likely to be related to muscle tension. 

Mr H didn’t see Dr P again for another two years. When he re-presented to Dr P, it was mainly to discuss some terminal dysuria. He mentioned that the headaches had been ongoing for two years and were still associated with vomiting. Dr P arranged for an MSU and bloods to be taken (CRP, LFTs, PV and PSA) and commenced sumatriptan to treat the headaches as migraine. Blood pressure was not checked. 

Mr H was reviewed the following week and investigations were all normal. His headache also appeared to have improved. Three months later, Mr H returned about his headaches again. He felt sumatriptan was no longer effective and requested a trial of physiotherapy to address his muscle tension. This was arranged, along with pain clinic review, and the patient was not seen by Dr P for another six months, until he presented with a presumed sinus infection. 

His blood pressure was recorded as 180/100 on this occasion, and when repeated a week later was still elevated at 166/110. Lisinopril was started at 5mg once daily. This was continued until he saw Dr P again four months later with symptoms of a UTI. Blood pressure was documented as 150/96 and lisinopril was doubled to a dose of 10mg daily. 

Time went on, and apart from a blood pressure check with the practice nurse every couple of months, Mr H was not followed up until seven months later when he was called in for some routine blood tests. His renal function was notably impaired with a serum creatinine of 262 umol/l, an eGFR of 23 ml/ min and a urea of 17.3 mmol/l. Investigations were initiated (renal USS was normal) and he was reviewed by consultant nephrologist Dr C. 

Dr C made note of recurrent UTIs during Mr H’s childhood and his hypertension, and concluded that reflux nephropathy was the most likely culprit. Dr C commented that it was likely that Mr H already had significant renal impairment when his hypertension was originally diagnosed, and although it would have been good practice to have checked renal function at this time, it was unlikely to have affected his outcome significantly. 

He further noted that the main tool available to delay renal deterioration is optimal control of blood pressure, using renal protective drugs like the lisinopril Mr H was given. 

Mr H made a claim against Dr P for alleged breach of duty – stating that renal function could have been tested on several occasions. Mr H also claimed for causation, stating that had renal function been tested when he first presented with headaches, then he would have been diagnosed at a far earlier stage, which would have allowed him to retain his renal function by a judicious use of medication and diet.

Expert opinion

Expert opinion was supportive of Dr P’s initial management. When Mr H first presented with headaches he had a single mildly elevated blood pressure reading followed by two normal results, which would not be consistent with a headache secondary to malignant hypertension or renal disease.

Although outside his area of expertise to comment on a GP’s standard of care, he did comment on Dr P’s failure to follow up Mr H more intensively once his hypertension was diagnosed and for failing to assess baseline renal function in conjunction with starting lisinopril. However, since the treatment to delay renal deterioration is to use an ACE inhibitor, experts agreed that on the balance of probabilities, earlier intervention is unlikely to have significantly affected Mr H’s long-term renal prognosis.

Mr H subsequently discontinued his claim.